Immune Response

views updated May 29 2018

Immune response

Definition

The action taken by the body to defend itself from pathogens or abnormalities is called the immune response. With the aid of the immune system , the body monitors constant exposure to harmful elements in the external and internal environment and provides a means of defense. Pathogens that are able to cause immune responses included bacteria , viruses , and parasites. The immune system must be able to determine what is a normal part of the body or "self," as opposed to that which is foreign or "non-self." The development of cancers, for example, represents a part of "self" that has been abnormally changed such that it is recognized as foreign to the immune system.

Description

The immune response can be roughly divided into two broad categories, innate (natural) immunity and adaptive (acquired) immunity. Innate immunity is the first line of defense against invasion by pathogens. This response is not directed against any one particular pathogen but is a capable of destroying many different invaders. If the pathogen is able to conquer this initial protection, an adaptive immune response will follow. In this response, lymphocytes arise that can specifically kill the invader and prevent re-infection. These lymphocytes recognize specific antigens on pathogens (substances that are foreign to the host cell and cause the production of antibodies to fight the disease).

Innate (natural) immunity

Innate immunity refers to those parts of the immune system that are normally present and do not given an elevated response upon a second exposure to a pathogen (without immunological memory ). This immunity is non-specific and is not directed against one type of pathogen. It is more generalized to allow the recognition of common elements that may be shared among pathogenic microorganisms.

Anatomical or physical barriers provide innate protection. The skin provides a protective barrier and contains substances that are antimicrobial (against bacterial growth) such as lactic acid, ammonia, and uric acid. The bacteria (microflora) that normally inhabit the skin do not cause disease under normal conditions. These organisms also contribute to innate immunity. The competition of the microflora with pathogens for resources and nutrients limits the growth of pathogens. If the skin is broken due to wounds or burns , pathogenic bacteria may enter to cause disease. In the urinary and biliary tracts, the increased flow of secretions provides protection against the establishment of harmful organisms.

Physiologic barriers are also a part of the innate immune system. Stomach acid can kill and inhibit the growth of many microorganisms and degrade potentially harmful proteins . A rise in body temperature can create an environment that is no longer suitable for the growth of some bacteria. Saliva, nasal secretions, tears, and mucus also contain substances that block viruses and help in the destruction of harmful bacteria.

Some cells of the immune system are able to attack and engulf pathogens, molecules, or particles by a process known as phagocytosis. The Russian immunologist Eli Metchnikoff observed that some pathogenic microorganisms were destroyed by phagocytic cells he called macrophages. These phagocytic cells originate in the bone marrow, are called monocytes in the bloodstream, and become macrophages in the tissue. These phagocytic macrophages in the tissue are able to ingest and destroy some pathogens even though they have not previously encountered them. These cells are capable of migration and are found in many sites throughout the body, including the lymph nodes, spleen, liver , lungs , as well as the peritoneal lining that surrounds the organs and the lungs. Macrophages in the bone are called osteoclasts, in the central nervous system they are called microglia, and in the connective tissue they are known as histiocytes. The neutrophils (polymorphonuclear leukocytes or PMNs) are another type of phagocytic cell that is critically important for innate immunity. These cells are found in great numbers and are one of the most important types of white blood cells found in the bloodstream. They are quickly recruited to the site of infection to engulf pathogens. Both neutrophils and macrophages contain enzymes that break down the engulfed material.

Natural killer (NK) cells are a type of lymphocyte in the blood that can detect and destroy cells infected by certain viruses. Viruses attack host cells and use them to facilitate viral replication and production of more viruses. Infected host cells must be rapidly destroyed to prevent this replication and spread of disease. It has been observed that natural killer cells play an especially important role in the early defense against herpes viruses. They also are involved in the killing of some tumors. Natural killer cells may kill by activating a process called apoptosis, the programmed cell death that is present in all cells and is responsible for their self-destruction.

The plasma contains a group of proteins called complements that act in a coordinated manner to attack pathogens. When some pathogens bind with a complement protein called C3b, a series of reactions in the alternative complement pathway occur. The surface of the pathogen is changed so that phagocytic cells can ingest them, a process called opsinization.

If the pathogen is able to effectively cross the barriers of innate immunity, an early induced, non-adaptive response will occur. This response serves to stop pathogens or slow them down until the body can initiate an adaptive immune response. Additional phagocytic cells and molecules are summoned to the site of infection by cytokines, a group of proteins that affect the actions of other cells. Some cytokines can cause an increase in the number of neutrophils in the circulation and fever , an elevation in body temperature. As most pathogenic bacteria have optimal growth at lower temperatures, this temperature rise helps to inhibit their growth. The fever also enhances the adaptive immune responses that follow. Local effects from injury or infection give rise to inflammation as white blood cells, fluid, and plasma proteins gather at the site. This is evident clinically at the site by redness, pain , heat, and swelling. The blood vessels in the site of injury or infection increase in diameter and allow more blood to flow into the area at a slower rate. Immune cells arrive quickly to the site and move into the tissue from the bloodstream. Small proteins called chemokines assist in this process and enhance the migration and activation of cells. Other special proteins called interferons are produced by virally infected cells and may stop the virus from multiplying within other cells, preventing the spread of infection.

Adaptive (acquired) immunity

In adaptive immunity, the immune response is specific for a particular antigen, causes lymphocytes that recognize the antigen to multiply (clonal expansion), and imparts the quality of immunological memory of prior encounters with the antigen. Specificity is an essential component of adaptive immunity as many organisms have evolved to evade the innate immune system. A system of defense is needed to specifically eliminate these elusive invaders, of which there are countless numbers. Two parts of adaptive immunity meet this challenge: cellular-mediated immunity and humoral (antibody-mediated immunity).

CELL-MEDIATED IMMUNITY. Once a pathogen has evaded the innate immune system, the cellular immune response mechanisms are initiated. In the lymphoid tissues, naive lymphocytes that have not been exposed to the pathogen encounter pathogen antigens for the first time. Dendritic cells, macrophages, and B cells take up the antigens that have been trapped in the lymphoid tissue and present them to naïve T cells. These T cells become activated, recognizing specific antigens from the pathogen and become effector cells; helper T cells (TH1 or TH2) and cytotoxic T cells. The TH1 cells produce interferons and cytokines that assist in the activation of macrophages that have ingested pathogens. They also help B cells make antibodies that are used to opsinize pathogens and secrete cytokines that draw phagocytic cells to the site of infection. The TH2 cells produce B cell growth factors that activate the B cells, causing them to multiply and produce antibodies that give rise to a humoral (antibody) response. A delicate balance exists between the TH1 and TH2 cells and is directed by cytokines. Cytotoxic T cells are involved in the killing of pathogens that live inside host cells (cytosolic pathogens) such as viruses and some bacteria. These pathogens hide within cells, and cannot be reached with antibodies. Cytotoxic T cells cause infected cells to undergo programmed cell death or apoptosis and also secrete cytokines that assist in the immune response.

HUMORAL (ANTIBODY-MEDIATED) IMMUNITY. The humoral immune response uses antibodies produced by B cells to destroy pathogens. Pathogens travel in the extracellular fluid (outside of the cell) during the spread of infection. Antibodies specific for foreign pathogen antigens combine with them and neutralize the pathogen, preventing the spread of infection. Toxins secreted by bacteria, such as those from diphtheria and tetanus, are harmful to the body may also be neutralized by antibodies. Bacterial surfaces may be coated with antibody such that phagocytic cells can recognize them and ingest them (opsinization). When antibodies bind with pathogen antigens, the complement system of plasma proteins is activated. This results in opsinization and draws phagocytes to the site of infection.

The B cells are activated upon exposure to antigen, such as that which occurs in the lymphoid tissue. B cell surfaces contain immunoglobulin proteins (antibody) that bind with antigens from pathogens. With the aid of antigen-specific helper T cells, the B cells begin to multiply and produce cells that make antibody (plasma cells). This antibody is directed against the same specific antigen that was recognized by the helper T cell. Memory B cells are also produced and are involved in the protection of the body upon a second exposure to the pathogen at another time. Some pathogens can also cause the B cells to become activated without the help of T cells.

Role in human health

Pathogens have evolved over time such that they can avoid detection by the immune system. Bacteria may change their antigens to escape recognition by immune cells. Such mechanisms occur in the case of bacteria that cause pneumonia , food poisoning , and gonorrhea. Theinfluenza virus may undergo a similar process, hence the reason that new flu vaccines are continually under development. The protozoans that cause malaria and sleeping sickness also use such methods to escape detection. Epstein-Barr and herpes simplex viruses enter a period of latency within the cells in which the virus does not multiply. The disease is "hidden" from immune surveillance, yet persists in the system to become active at a later time.

In opportunistic infections, a microorganism that is normally present as part of the microflora is no longer controlled by the host and seizes an opportunity to establish infection. This occurs in HIV infection due to suppressed immunity in the body. Opportunistic infections may arise following medical or surgical treatments. Such is the case with urinary tract infections when Esherichia coli that are normally found on the gut enter the urinary tract during catheterization or yeast infections following the administration of antibiotics .

Immune responses are particularly important during the process of organ transplantation where the recipient may perceive donor antigens as "non-self." Careful matching of donor and recipient tissues and the use of immunosuppressive agents that diminish the immune response minimize rejection. Graft-vs-host disease occurs during bone marrow transplants when the T cells of the donor recognize antigens in the recipient as "foreign."

Directions in immunotherapy

Humans have tried to understand the immune response and prevent the spread of disease throughout history. In ancient China and Asia Minor, attempts were made to inoculate against the smallpox virus by a process called variolization. In 1774 a farmer, Benjamin Jesty, used the cowpox virus to protect his children from smallpox. Edward Jenner began studies using cowpox virus in 1796 and demonstrated that immunization with cowpox protected a child from developing a smallpox infection. He published his results, calling this process vaccination . Efforts to refine this process ultimately lead to the declaration by the World Health Organization 1979 that the disease had been eradicated. Research directions for 2000 and beyond include vaccine development for HIV, tumors, schitosomiasis (a parasitic disease), and malaria.

Advances in cytokine therapy are another promising area of research and development. This approach involves boosting the body's own immune modulators to initiate an increased response. The use of cytokines has been explored in bone marrow transplantation, sepsis trials, and treatment of leprosy.


KEY TERMS


Adaptive immunity —The immune response is specific for a particular antigen, causes lymphocytes that recognize the antigen to multiply (clonal expansion), and imparts the quality of immunological memory of prior encounters with the antigen.

Apoptosis —The programmed cell death that is present in all cells and is responsible for their self-destruction.

Innate immunity —Parts of the immune system that are normally present, non-specific, and do not given an elevated response upon a second exposure.

Phagocytosis —The process whereby a cell engulfs particles or materials.


Resources

BOOKS

Anderson, William L. Immunology. Madison, CT: Fence Creek Publishing, 1999.

Janeway, Charles A., et al. Immunobiology: The Immune System in Health and Disease. London and New York: Elsevier Science London/Garland Publishing, 1999.

Levine, M., et al.,eds., New Generation Vaccines. New York: Marcel Dekker, 1997.

Roitt, Ivan, and Arthur Rabson. Really Essential Medical Immunology. Malden: Blackwell Science, 2000.

Sharon, Jacqueline. Basic Immunology. Baltimore, MD: Williams and Wilkins, 1998.

Widmann, Frances K., and Carol A. Itatani An Introduction to Clinical Immunology and Serology. Philadelphia, PA: F.A. Davis Company, 1998.

Wier, Donald M., and John Stewart. Immunology. New York: Churchchill Livingstone, Inc., 1997.

OTHER

Mayo Clinic Website. <http://www.mayoclinic.com>.

Med Web, Emory University. <http://www.medweb.emory.edu/MedWeb/>.

Med Web, Medem. <http://www.medem.com>.

The Vaccine Page. <http://www.vaccines.com>.

Jill Ilene Granger, M.S.

Immune Response

views updated May 23 2018

Immune Response

Definition

The action taken by the body to defend itself from pathogens or abnormalities is called the immune response. With the aid of the immune system, the body monitors constant exposure to harmful elements in the external and internal environment and provides a means of defense. Pathogens that are able to cause immune responses included bacteria, viruses, and parasites. The immune system must be able to determine what is a normal part of the body or "self," as opposed to that which is foreign or "non-self." The development of cancers, for example, represents a part of "self" that has been abnormally changed such that it is recognized as foreign to the immune system.

Description

The immune response can be roughly divided into two broad categories, innate (natural) immunity and adaptive (acquired) immunity. Innate immunity is the first line of defense against invasion by pathogens. This response is not directed against any one particular pathogen but is a capable of destroying many different invaders. If the pathogen is able to conquer this initial protection, an adaptive immune response will follow. In this response, lymphocytes arise that can specifically kill the invader and prevent re-infection. These lymphocytes recognize specific antigens on pathogens (substances that are foreign to the host cell and cause the production of antibodies to fight the disease).

Innate (natural) immunity

Innate immunity refers to those parts of the immune system that are normally present and do not give an elevated response upon a second exposure to a pathogen (without immunological memory ). This immunity is non-specific and is not directed against one type of pathogen. It is more generalized to allow the recognition of common elements that may be shared among pathogenic microorganisms.

Anatomical or physical barriers provide innate protection. The skin provides a protective barrier and contains substances that are antimicrobial (against bacterial growth) such as lactic acid, ammonia, and uric acid. The bacteria (microflora) that normally inhabit the skin do not cause disease under normal conditions. These organisms also contribute to innate immunity. The competition of the microflora with pathogens for resources and nutrients limits the growth of pathogens. If the skin is broken due to wounds or burns, pathogenic bacteria may enter to cause disease. In the urinary and biliary tracts, the increased flow of secretions provides protection against the establishment of harmful organisms.

Physiologic barriers are also a part of the innate immune system. Stomach acid can kill and inhibit the growth of many microorganisms and degrade potentially harmful proteins. A rise in body temperature can create an environment that is no longer suitable for the growth of some bacteria. Saliva, nasal secretions, tears, and mucus also contain substances that block viruses and help in the destruction of harmful bacteria.

Some cells of the immune system are able to attack and engulf pathogens, molecules, or particles by a process known as phagocytosis. The Russian immunologist Eli Metchnikoff observed that some pathogenic microorganisms were destroyed by phagocytic cells he called macrophages. These phagocytic cells originate in the bone marrow, are called monocytes in the bloodstream, and become macrophages in the tissue. These phagocytic macrophages in the tissue are able to ingest and destroy some pathogens even though they have not previously encountered them. These cells are capable of migration and are found in many sites throughout the body, including the lymph nodes, spleen, liver, lungs, as well as the peritoneal lining that surrounds the organs and the lungs. Macrophages in the bone are called osteoclasts, in the central nervous system they are called microglia, and in the connective tissue they are known as histiocytes. The neutrophils (polymorphonuclear leukocytes or PMNs) are another type of phagocytic cell that is critically important for innate immunity. These cells are found in great numbers and are one of the most important types of white blood cells found in the bloodstream. They are quickly recruited to the site of infection to engulf pathogens. Both neutrophils and macrophages contain enzymes that break down the engulfed material.

Natural killer (NK) cells are a type of lymphocyte in the blood that can detect and destroy cells infected by certain viruses. Viruses attack host cells and use them to facilitate viral replication and production of more viruses. Infected host cells must be rapidly destroyed to prevent this replication and spread of disease. It has been observed that natural killer cells play an especially important role in the early defense against herpes viruses. They also are involved in the killing of some tumors. Natural killer cells may kill by activating a process called apoptosis, the programmed cell death that is present in all cells and is responsible for their self-destruction.

The plasma contains a group of proteins called complements that act in a coordinated manner to attack pathogens. When some pathogens bind with a complement protein called C3b, a series of reactions in the alternative complement pathway occur. The surface of the pathogen is changed so that phagocytic cells can ingest them, a process called opsinization.

If the pathogen is able to effectively cross the barriers of innate immunity, an early induced, non-adaptive response will occur. This response serves to stop pathogens or slow them down until the body can initiate an adaptive immune response. Additional phagocytic cells and molecules are summoned to the site of infection by cytokines, a group of proteins that affect the actions of other cells. Some cytokines can cause an increase in the number of neutrophils in the circulation and fever, an elevation in body temperature. As most pathogenic bacteria have optimal growth at lower temperatures, this temperature rise helps to inhibit their growth. The fever also enhances the adaptive immune responses that follow. Local effects from injury or infection give rise to inflammation as white blood cells, fluid, and plasma proteins gather at the site. This is evident clinically at the site by redness, pain, heat, and swelling. The blood vessels in the site of injury or infection increase in diameter and allow more blood to flow into the area at a slower rate. Immune cells arrive quickly to the site and move into the tissue from the bloodstream. Small proteins called chemokines assist in this process and enhance the migration and activation of cells. Other special proteins called interferons are produced by virally infected cells and may stop the virus from multiplying within other cells, preventing the spread of infection.

Adaptive (acquired) immunity

In adaptive immunity, the immune response is specific for a particular antigen, causes lymphocytes that recognize the antigen to multiply (clonal expansion), and imparts the quality of immunological memory of prior encounters with the antigen. Specificity is an essential component of adaptive immunity as many organisms have evolved to evade the innate immune system. A system of defense is needed to specifically eliminate these elusive invaders, of which there are countless numbers. Two parts of adaptive immunity meet this challenge: cellular-mediated immunity and humoral (antibody-mediated immunity).

CELL-MEDIATED IMMUNITY. Once a pathogen has evaded the innate immune system, the cellular immune response mechanisms are initiated. In the lymphoid tissues, naive lymphocytes that have not been exposed to the pathogen encounter pathogen antigens for the first time. Dendritic cells, macrophages, and B cells take up the antigens that have been trapped in the lymphoid tissue and present them to naïve T cells. These T cells become activated, recognizing specific antigens from the pathogen and become effector cells; helper T cells (TH1 or TH2) and cytotoxic T cells. The TH1 cells produce interferons and cytokines that assist in the activation of macrophages that have ingested pathogens. They also help B cells make antibodies that are used to opsinize pathogens and secrete cytokines that draw phagocytic cells to the site of infection. The TH2 cells produce B cell growth factors that activate the B cells, causing them to multiply and produce antibodies that give rise to a humoral (antibody) response. A delicate balance exists between the TH1 and TH2 cells and is directed by cytokines. Cytotoxic T cells are involved in the killing of pathogens that live inside host cells (cytosolic pathogens) such as viruses and some bacteria. These pathogens hide within cells, and cannot be reached with antibodies. Cytotoxic T cells cause infected cells to undergo programmed cell death or apoptosis and also secrete cytokines that assist in the immune response.

HUMORAL (ANTIBODY-MEDIATED) IMMUNITY. The humoral immune response uses antibodies produced by B cells to destroy pathogens. Pathogens travel in the extracellular fluid (outside of the cell) during the spread of infection. Antibodies specific for foreign pathogen antigens combine with them and neutralize the pathogen, preventing the spread of infection. Toxins secreted by bacteria, such as those from diphtheria and tetanus, are harmful to the body may also be neutralized by antibodies. Bacterial surfaces may be coated with antibody such that phagocytic cells can recognize them and ingest them (opsinization). When antibodies bind with pathogen antigens, the complement system of plasma proteins is activated. This results in opsinization and draws phagocytes to the site of infection.

The B cells are activated upon exposure to antigen, such as that which occurs in the lymphoid tissue. B cell surfaces contain immunoglobulin proteins (antibody) that bind with antigens from pathogens. With the aid of antigen-specific helper T cells, the B cells begin to multiply and produce cells that make antibody (plasma cells). This antibody is directed against the same specific antigen that was recognized by the helper T cell. Memory B cells are also produced and are involved in the protection of the body upon a second exposure to the pathogen at another time. Some pathogens can also cause the B cells to become activated without the help of T cells.

Role in human health

Pathogens have evolved over time such that they can avoid detection by the immune system. Bacteria may change their antigens to escape recognition by immune cells. Such mechanisms occur in the case of bacteria that cause pneumonia, food poisoning, and gonorrhea. The influenza virus may undergo a similar process, hence the reason that new flu vaccines are continually under development. The protozoans that cause malaria and sleeping sickness also use such methods to escape detection. Epstein-Barr and herpes simplex viruses enter a period of latency within the cells in which the virus does not multiply. The disease is "hidden" from immune surveillance, yet persists in the system to become active at a later time.

In opportunistic infections, a microorganism that is normally present as part of the microflora is no longer controlled by the host and seizes an opportunity to establish infection. This occurs in HIV infection due to suppressed immunity in the body. Opportunistic infections may arise following medical or surgical treatments. Such is the case with urinary tract infections when Esherichia coli that are normally found on the gut enter the urinary tract during catheterization or yeast infections following the administration of antibiotics.

Immune responses are particularly important during the process of organ transplantation where the recipient may perceive donor antigens as "non-self." Careful matching of donor and recipient tissues and the use of immunosuppressive agents that diminish the immune response minimize rejection. Graft-vs-host disease occurs during bone marrow transplants when the T cells of the donor recognize antigens in the recipient as "foreign."

Directions in immunotherapy

Humans have tried to understand the immune response and prevent the spread of disease throughout history. In ancient China and Asia Minor, attempts were made to inoculate against the smallpox virus by a process called variolization. In 1774 a farmer, Benjamin Jesty, used the cowpox virus to protect his children from smallpox. Edward Jenner began studies using cowpox virus in 1796 and demonstrated that immunization with cowpox protected a child from developing a smallpox infection. He published his results, calling this process vaccination. Efforts to refine this process ultimately lead to the declaration by the World Health Organization 1979 that the disease had been eradicated. Research directions for 2000 and beyond include vaccine development for HIV, tumors, schitosomiasis (a parasitic disease), and malaria.

Advances in cytokine therapy are another promising area of research and development. This approach involves boosting the body's own immune modulators to initiate an increased response. The use of cytokines has been explored in bone marrow transplantation, sepsis trials, and treatment of leprosy.

KEY TERMS

Adaptive immunity— The immune response is specific for a particular antigen, causes lymphocytes that recognize the antigen to multiply (clonal expansion), and imparts the quality of immunological memory of prior encounters with the antigen.

Apoptosis— The programmed cell death that is present in all cells and is responsible for their self-destruction.

Innate immunity— Parts of the immune system that are normally present, non-specific, and do not given an elevated response upon a second exposure.

Phagocytosis— The process whereby a cell engulfs particles or materials.

Resources

BOOKS

Anderson, William L. Immunology. Madison, CT: Fence Creek Publishing, 1999.

Janeway, Charles A., et al. Immunobiology: The Immune System in Health and Disease. London and New York: Elsevier Science London/Garland Publishing, 1999.

Levine, M., et al., eds., New Generation Vaccines. New York: Marcel Dekker, 1997.

Roitt, Ivan, and Arthur Rabson. Really Essential Medical Immunology. Malden: Blackwell Science, 2000.

Sharon, Jacqueline. Basic Immunology. Baltimore, MD: Williams and Wilkins, 1998.

Widmann, Frances K., and Carol A. Itatani. An Introduction to Clinical Immunology and Serology. Philadelphia, PA: F.A. Davis Company, 1998.

Wier, Donald M., and John Stewart. Immunology. New York: Churchchill Livingstone, Inc., 1997.

OTHER

Mayo Clinic Website. 〈http://www.mayoclinic.com〉.

Med Web, Emory University. 〈http://www.medweb.emory.edu/MedWeb/〉.

Med Web, Medem. 〈http://www.medem.com〉.

The Vaccine Page. 〈http://www.vaccines.com〉.

Immune Response

views updated May 21 2018

Immune Response

Among the many threats organisms face are invasion and infection by bacteria, viruses, fungi, and other foreign or disease-causing agents. All organisms have nonspecific defenses (or innate defenses) that provide them with some of the protection they need. This type of defense exists throughout the animal kingdom, from sponges to mammals. Vertebrate animals, however, have an additional line of defense called specific immunity. Specific immunity is also called acquired immunity, adaptive immunity, or, most simply, an immune response.

Overview

One characteristic of specific immunity is recognition. Immune responses begin when the body recognizes the invader as foreign. This occurs because there are molecules on foreign cells that are different from molecules on the body's cells. Molecules that start immune responses are called antigens . The body does not usually start an immune response against its own antigens because cells that recognize self-antigens are deleted or inactivated. This concept is called self-tolerance and is a key characteristic that defines immune responses.

A second characteristic is specificity. Although all immune responses are similar, each time the body is invaded by a different antigen, the exact response is specific to that antigen. For example, infection with a virus that causes the common cold triggers a response by a different set of cells than infection with bacteria that causes strep throat.

A third characteristic is memory. After an antigen is cleared from the body, immunological memory allows an antigen to be recognized and removed more quickly if encountered again.

Antigen Presentation

Three groups of white blood cells are involved in starting an immune response. Although immune responses can occur anywhere in the body these cells are found, they primarily occur in the lymph nodes and spleen. These organs contain large numbers of antigen-presenting cells (APCs), T lymphocytes (or T cells ), and B lymphocytes (or B cells).

APCs include macrophages, dendritic cells, and B cells. These cells encounter the foreign invader and present the invader's antigens to a group of T cells called helper T cells (TH cells). APCs do this by first engulfing an invader and bringing it inside the cell. The APC then breaks the invader apart into its antigens and moves these antigens to its cell surface.

Receptors are cell surface proteins that can attach to antigens. Each TH cell has a different receptor, allowing each cell to recognize a different antigen. The APC "shows" the antigen to the TH cells until there is a match between a TH cell receptor and the antigen. The contact between the two cells stimulates the TH cell to divide rapidly. This process is called clonal selection because only the TH cells that recognize the foreign invader are selected to reproduce. Stimulated TH cells also produce chemical messengers called cytokines. Cytokines are made by all immune cells and control the immune response.

Antigen Clearance

The large numbers of TH cells activate two other populations of white blood cells: cytotoxic T cells (TC cells) and B cells. Like TH cells, each TC cell and B cell has receptors that match one antigen. This is why the immune system can recognize millions of antigens with specificity. The cells with the appropriate receptor encounter the antigen, preparing them for activation. They receive the final signal necessary for clonal selection from TH cells and cytokines.

Cloned TC cells attach to invaders they recognize and release a variety of chemicals that destroy the foreign cell. Because this must happen through cell-to-cell contact, it is called cell-mediated immunity (or cellular immunity). It is especially effective at destroying abnormal body cells, such as cancerous cells or virus-infected cells.

Cloned B cells destroy foreign invaders differently. After activation by TH cells, B cells release proteins called antibodies. Antibodies travel through the body's fluids and attach to antigens, targeting them for destruction by nonspecific defenses. This type of immune response is called antibody -mediated immunity (or humoral immunity). It is especially effective at destroying bacteria, extracellular viruses, and other antigens found in body fluids.

Immunologic Memory

A primary immune response happens the first time that the body encounters a specific antigen. It takes several days to begin and one or two weeks to reach maximum activity. A secondary immune response occurs if the body encounters the same antigen at a later time. It takes only hours to begin and may peak within a few days. The invader is usually removed before it has a chance to cause disease. This is because some of the cloned TC cells and B cells produced during a primary immune response develop into memory cells. These cells immediately become activated if the antigen appears again. The complex interactions among cells described above are not necessary.

In fact, this is what happens when an individual is immunized against a disease. The vaccination (using weakened or killed pathogens ) causes a primary immune response (but not the disease) and the production of memory cells that will provide protection if exposed to the diseasecausing agent.

Immune System Disorders

Studying immune responses also allows scientists to understand immune system diseases. For example, hypersensitivity disorders occur when the immune system overreacts to an antigen, causing damage to healthy tissues. The result of this excessive antibody and TC cell activity can be relatively harmless (as with allergies to pollen, poison ivy, or molds) or deadly (as with autoimmune diseases or allergies to bee venom and antibiotics).

At the opposite end of the spectrum are immunodeficiency diseases, conditions in which the body does not respond effectively against foreign invaders. HIV (human immunodeficiency virus) infection causes AIDS (acquired immunodeficiency syndrome) by attacking TH cells. Occasionally an individual is born with a deficient immune system, but these disorders are usually acquired (for example, from radiation treatment, chemotherapy, or infection with HIV). Whatever the cause, the individual has a more difficult time fighting infections.

Because immune responses exhibit the characteristics of self-tolerance, specificity, and memory, a healthy body is well equipped to remove foreign invaders and prevent recurrent infections. Age, nutrition, exercise, and stress all affect the ability of the body to fight disease.

see also AIDS; Antibody; Autoimmune Disease; Nonspecific Defense

John M. Ripper

Bibliography

Beck, Gregory, and Gail S. Habicht. "Immunity and the Invertebrates." Scientific American 275, no. 5 (1996): 6065.

Friedlander, Mark P., Jr., and Terry M. Phillips. The Immune System: Your Body's Disease-Fighting Army. Minneapolis, MN: Lerner Publications Company, 1998.

Gustav, J. V. "Life, Death, and the Immune System." Scientific American 269, no. 3 (1993): 5362.

National Institutes of Health. Understanding the Immune System. Washington, DC: National Institutes of Health, 1993.

Paul, William. E. "Infectious Diseases and the Immune System." Scientific American 269, no. 3 (1993): 9097.

Immune Response

views updated May 14 2018

Immune response

Definition

The ability of any given cell in the body to distinguish self from nonself is called the immune response.

All cells in the body are recognized as self. Any microorganism (for example, a foreign body or tumor) that invades or attacks the cells is recognized as nonselfor foreignrequiring the immune system to mount a combat against the nonself.

Immune system

The immune system is comprised of a network of immune cells that are generated in the bone marrow stem cell (a cell whose daughter cells may develop into other types of cells). From stem cells different types of immune cells originate that can handle specific immune functions. Phagocytes (cell eaters), serve as the first line of defense, engulfing dead cells, debris, virus, and bacteria. Macrophages are an important type of phagocyte, often presenting the antigenwhich is usually a foreign proteinto other immune cells and thus are also called "antigen-presenting cells" (APC). T and B lymphocytes, important immune-system cells, are also capable of recognizing the antigen and become activated. T lymphocytes are classified into two subtypes: killer T cells (also called cytotoxic T cells) and helper T cells. Killer T cells recognize and kill the infected or cancer cells that contain the antigen or the foreign protein. Helper T cells release cytokines (chemical messengers) upon activation that either directly destroy the tumor or stimulate other cells to kill the target (tumor). B lymphocytes produce antibodies after recognizing the antigens. The antibodies, which help protect the body from the antigen, are normally specific to that particular antigen. In cases of tumor the specific antibodies attach to tumor cells and, through various mechanisms, impair the functions of the tumor, ultimately leading to the death of the cancer cell.

In addition to these lymphocytes are natural killer (NK) cells that particularly perform the task of eliminating foreign cells. Natural killer cells differ from killer T cells in that they target tumor cells and do not have to recognize an antigen before activation. These cells have been shown to be of potential use in treating cancer.

Immune system and cancer

The immune system serves as one of the primary defenses against cancer. When normal tissue becomes a tumor or cancerous tissue, new antigens develop on their surface. These antigens send a signal to immune cells such as the cytotoxic T lymphocytes, NK cells, and macrophages, which in turn directly kill the tumor cells or release substances like cytokines that may bring about tumor cell death. Thus, under normal circumstances, the immune system provides continued surveillance and eliminates cells that become cancers. However, tumors may survive by hiding or disguising their tumor antigens, or by producing substances that allow suppressor T cells (cells that block cytotoxic, or killer T cells that would normally attack the tumor) to proliferate (multiply).

Biological response modifiers in cancer therapy

Researchers have been working on stimulating the immune cells during cancer with substances broadly classified as biological response modifiers. Cytokines are one such substance. These are proteins that are predominantly released by immune cells upon activation or stimulation. During the 1990s the number of cytokines identified increased enormously and the functions associated with them are of immense potential in diagnostics and immune therapy. Some of the key cytokines that have proven therapeutic value in cancer are interleukin-2 (IL-2), Interferon gamma, and interleukin-12 (IL-12). Cytokines are normally injected directly to cancer patients; however, there are other cases where a cancer patient's own lymphocytes are modified under laboratory conditions and injected back into the patient. Examples of these are lymphokine-activated killer (LAK) cells and tumor-infiltrating lymphocytes (TILs). These modified cells are capable of devouring cancer cells.

Immunoprevention of cancer

Immunotherapy is emerging as one of the management strategies for cancer. However, established tumors or large masses of tumor do not respond well to immunotherapy. There is clinical evidence, however, that suggests that patients with minimal residual cancer cells (a few cells left after other forms of cancer treatment) are potential candidates for effective immunotherapy. In these cases immunotherapy often results in a prolonged tumor-free survival. Thus, immune responses can be manipulated to prevent recurrence, even though it does not destroy large tumors. Based on results of immunotherapy trials, most immune therapies are geared towards designing immunoprotective strategies such as cancer vaccines .

Cancer vaccines

Cancer vaccines can be made either with whole, inactivated tumor cells, or with fragments or cell surface substances (called cell-surface antigens) present in the tumors. In addition to the whole cell or antigen vaccines, biological modifiers, like cytokines, serve as substances that boost immune response in cancer patients.

Since cancer vaccines are still under clinical evaluation, caution should be exercised while choosing them as the mode of therapy. The cancer care team will provide further insight on whether or not cancer vaccine or cytokine therapy will be beneficial after they assess the patient's stage and the various modes of treatments available.

Kausalya Santhanam, Ph.D.

Resources

BOOKS

DeVita, Vincent T., Samuel Hellman, and Steven A. Rosenberg, eds. Cancer: Principles and Practice of Oncology. Philadelphia: J. B. Lippincott Company, 1997.

PERIODICALS

"Immunoprevention of Cancer: Is the Time Ripe?" Cancer Research (15 May 2000) 60: 2571-2575

"Therapies of the Future: Immunotherapy for Cancer." Scientific American (October 1996).

"Genetic Vaccines." Scientific American (July 1999).

OTHER

"Treating Cancer with Vaccine Therapy." National Cancer Institute. 2000. 5 July 2001 <http://cancertrials.nci.nih.gov/news/features/vaccine/html/page05.html>.

KEY TERMS

Antigen

Molecules or fragments of molecules that belong to a foreign invader that can elicit an immune response. These may include germs, toxins, and tissues from another person used in organ transplantation.

Cytokines

Proteins (chemical messengers) that are predominantly released by immune cells upon activation or stimulation that help bring about tumor cell death.

Stem cell

A cell whose daughter cells may differentiate (develop into other cell types).

immune response

views updated May 23 2018

immune response The reaction of the body to foreign or potentially dangerous substances (antigens), particularly disease-producing microorganisms. The response involves the production by specialized white blood cells (B cells) of proteins known as antibodies, which react with the antigens to render them harmless (see immunoglobulin). The antibody–antigen reaction is highly specific. See also anaphylaxis; immunity.

immune response

views updated Jun 11 2018

im·mune re·sponse • n. the reaction of the cells and fluids of the body to the presence of a substance that is not recognized as a constituent of the body itself.