Types of antigen on the basis of source and immune response
Antigens are molecules that can be recognized by the immune system and trigger an immune response. The term antigen derives from the words "antibody generator". Antigens can be proteins, polysaccharides, lipids, nucleic acids, or any other substances that can bind to specific receptors on immune cells. Antigens can be classified into different types based on their source, origin, or the type of immune response they elicit.
The immune system is composed of two main branches: the innate immunity and the adaptive immunity. The innate immunity is the first line of defense against pathogens and foreign substances. It consists of physical barriers (such as skin and mucous membranes), chemical mediators (such as complement and interferons), and cellular components (such as macrophages, neutrophils, and natural killer cells). The innate immunity is fast, nonspecific, and does not have memory.
The adaptive immunity is the second line of defense that is activated by the recognition of specific antigens. It consists of two types of lymphocytes: B cells and T cells. B cells produce antibodies that bind to antigens and neutralize them or mark them for destruction. T cells can either help B cells to produce antibodies (helper T cells) or directly kill infected cells or cancer cells (cytotoxic T cells). The adaptive immunity is slow, specific, and has memory.
The recognition of antigens by the adaptive immunity involves two types of molecules: the major histocompatibility complex (MHC) and the antigen receptors. The MHC molecules are proteins that are expressed on the surface of most nucleated cells. They present fragments of antigens to T cells. There are two classes of MHC molecules: MHC class I and MHC class II. MHC class I molecules present endogenous antigens (antigens that originate from within the cell) to cytotoxic T cells. MHC class II molecules present exogenous antigens (antigens that originate from outside the cell) to helper T cells.
The antigen receptors are proteins that are expressed on the surface of B cells and T cells. They bind to specific antigens with high affinity and specificity. There are two types of antigen receptors: the B cell receptor (BCR) and the T cell receptor (TCR). The BCR is composed of two identical heavy chains and two identical light chains that form a Y-shaped structure. The variable regions at the tips of the Y-shaped structure form the antigen-binding site. The BCR can bind to free antigens in solution or on the surface of pathogens. The TCR is composed of one alpha chain and one beta chain that form a heterodimer. The variable regions at the ends of the alpha and beta chains form the antigen-binding site. The TCR can only bind to antigens that are presented by MHC molecules.
The interaction between antigens and antigen receptors initiates a cascade of signaling events that leads to the activation, proliferation, differentiation, and effector functions of B cells and T cells. The activated B cells and T cells can also form memory cells that can respond more quickly and effectively to subsequent encounters with the same antigen.
In this article, we will discuss the different types of antigens based on their source/origin and their immune response.
Antigens can be classified into different types based on their source or origin. The source or origin of an antigen determines how it enters the body, how it is processed and presented by the immune system, and what kind of immune response it elicits. The main types of antigens based on source or origin are:
Exogenous antigens: These are antigens that come from outside the body, such as bacteria, viruses, fungi, parasites, toxins, pollen, etc. They enter the body through various routes, such as inhalation, ingestion, injection, or skin contact. Exogenous antigens are usually captured and processed by antigen-presenting cells (APCs), such as macrophages and dendritic cells, which then display fragments of the antigens on their surface in association with major histocompatibility complex (MHC) molecules. These antigen-MHC complexes can then be recognized by T cells and B cells, which initiate the adaptive immune response.
Endogenous antigens: These are antigens that originate from within the body, such as normal or abnormal cells, tissues, or molecules. They can be generated as a result of normal cell metabolism, cellular stress, infection by intracellular pathogens, or transformation into cancerous cells. Endogenous antigens are usually processed and presented by infected or altered cells themselves in association with MHC class I molecules. These antigen-MHC class I complexes can then be recognized by cytotoxic T cells (CD8+ T cells), which can kill the infected or abnormal cells.
Autoantigens: These are antigens that are normally present in the body and do not elicit an immune response under normal conditions. However, in some cases, due to genetic or environmental factors, the immune system may lose its tolerance to these self-antigens and start attacking them as if they were foreign. This leads to autoimmune diseases, such as rheumatoid arthritis, type 1 diabetes mellitus, multiple sclerosis, etc. Autoantigens can be exogenous or endogenous in origin.
Some antigens can be both exogenous and endogenous depending on the context. For example, intracellular viruses can enter the body as exogenous antigens and then replicate inside the host cells and become endogenous antigens. Similarly, some proteins or nucleic acids can be both self and non-self depending on their location or modification. For example, DNA can be an autoantigen when it is released from damaged cells into the extracellular space or when it is modified by methylation or oxidation.
Exogenous antigens are antigens that enter the body from the outside, such as through inhalation, ingestion, or injection. These antigens are foreign to the host body and are also called foreign antigens. Examples of exogenous antigens include bacteria, fungi, viruses, pollen, dust, etc.
Exogenous antigens circulate in the body fluids and are trapped by the antigen-presenting cells (APCs), such as macrophages, dendritic cells, and B cells. The uptake of these exogenous antigens by APCs is mainly mediated by phagocytosis, a process of engulfing and digesting the antigens.
The APCs then process the exogenous antigens and present them on their surface in association with major histocompatibility complex (MHC) class II molecules. MHC class II molecules are proteins that display the antigen fragments to the helper T cells, a type of immune cell that recognizes and activates the immune response against the antigen.
The helper T cells then secrete cytokines, which are chemical messengers that stimulate other immune cells, such as B cells and cytotoxic T cells. B cells produce antibodies that bind to the exogenous antigens and mark them for destruction by other immune cells or complement proteins. Cytotoxic T cells kill the infected or abnormal cells that express the exogenous antigens on their surface.
Exogenous antigens are the main targets of humoral immunity, which is mediated by antibodies and complement proteins in the body fluids. Humoral immunity can neutralize and eliminate the extracellular pathogens and toxins that carry the exogenous antigens.
Endogenous antigens are antigens that originate from within the host`s own body. These are usually normal cellular components or products that are recognized by the immune system as foreign or abnormal. Endogenous antigens can also be produced by intracellular pathogens, such as viruses or bacteria, that infect the host cells and alter their antigenic properties.
The endogenous antigens are processed and presented by specialized cells called antigen-presenting cells (APCs), such as macrophages, dendritic cells, or B cells. The APCs degrade the endogenous antigens into smaller fragments called peptides and display them on their surface in association with major histocompatibility complex (MHC) class I molecules. The MHC class I-peptide complexes are then recognized by cytotoxic T lymphocytes (CTLs), which are a type of T cells that can kill infected or abnormal cells.
The endogenous antigen presentation pathway is important for the elimination of intracellular pathogens and cancer cells. It also plays a role in the induction of tolerance to self-antigens and the prevention of autoimmune diseases. However, some endogenous antigens can escape the immune surveillance and trigger an immune response against the host`s own tissues, leading to autoimmune disorders such as type 1 diabetes, multiple sclerosis, rheumatoid arthritis, or systemic lupus erythematosus. Therefore, the regulation of endogenous antigen processing and presentation is crucial for maintaining immune homeostasis and avoiding self-reactivity.
Autoantigens are antigens that are normally present in the body and do not elicit an immune response under normal conditions. However, in some cases, the immune system may lose its tolerance to these self-antigens and start attacking them as if they were foreign. This leads to autoimmune diseases, such as rheumatoid arthritis, type 1 diabetes, multiple sclerosis, lupus, and others.
The exact mechanisms that cause the breakdown of self-tolerance are not fully understood, but some factors that may contribute to it include genetic predisposition, environmental triggers, molecular mimicry, and epigenetic changes. Some examples of autoantigens are:
- Thyroglobulin: a protein that is involved in the synthesis of thyroid hormones. It is targeted by autoantibodies in Hashimoto`s thyroiditis and Graves` disease, which are autoimmune disorders of the thyroid gland.
- DNA: the genetic material of the cell. It is targeted by autoantibodies in systemic lupus erythematosus (SLE), which is a chronic inflammatory disease that can affect various organs and tissues.
- Corneal tissue: the transparent layer that covers the front of the eye. It is targeted by autoantibodies in Mooren`s ulcer, which is a rare and severe form of corneal inflammation.
- Insulin: a hormone that regulates blood glucose levels. It is targeted by autoantibodies in type 1 diabetes mellitus, which is a metabolic disorder characterized by high blood sugar and lack of insulin production.
Autoantigens can also be classified into two types based on their location:
- Tissue-specific autoantigens: these are antigens that are expressed only in certain tissues or organs, such as thyroglobulin or insulin. They can cause organ-specific autoimmune diseases, such as thyroiditis or diabetes.
- Systemic autoantigens: these are antigens that are widely distributed throughout the body, such as DNA or nuclear proteins. They can cause systemic autoimmune diseases, such as SLE or rheumatoid arthritis.
The diagnosis and treatment of autoimmune diseases depend on the type and severity of the condition, as well as the specific autoantigen involved. Some common methods include blood tests to detect autoantibodies, immunosuppressive drugs to reduce inflammation and immune activity, and replacement therapy to compensate for the loss of function of the affected organ or tissue.
Some antigens can have both exogenous and endogenous origins, depending on how they enter and interact with the host body. For example, intracellular viruses are exogenous antigens when they infect the host cells from outside, but they become endogenous antigens when they replicate inside the host cells and produce viral proteins that are presented on the cell surface by MHC class I molecules. Similarly, some bacteria can be exogenous antigens when they are phagocytosed by APCs and processed by MHC class II pathway, but they can also be endogenous antigens when they escape from the phagosome and enter the cytoplasm of the APCs, where they are processed by MHC class I pathway. Another example of antigens that can be both exogenous and endogenous are tumor antigens, which are derived from normal cellular proteins that are mutated or overexpressed in cancer cells. Tumor antigens can be exogenous when they are released from dying tumor cells and taken up by APCs, or endogenous when they are expressed on the surface of tumor cells by MHC class I molecules.
The distinction between exogenous and endogenous antigens is important for the activation of different types of immune cells. Exogenous antigens activate helper T cells (CD4+), which provide help to B cells for antibody production and to macrophages for enhanced phagocytosis. Endogenous antigens activate cytotoxic T cells (CD8+), which kill infected or abnormal cells by inducing apoptosis. Therefore, antigens that can be both exogenous and endogenous can elicit both humoral and cellular immune responses, depending on how they are presented to the immune system.
Another way to classify antigens is based on their ability to elicit an immune response. Not all antigens are equally immunogenic, meaning that some of them can trigger a specific and strong immune reaction, while others can only do so with the help of other molecules or cells. Depending on their immunogenicity, antigens can be divided into four main categories:
- Immunogens/Complete antigens: These are antigens that can induce a specific immune response by themselves, without the need of any other factors. They are usually large and complex molecules, such as proteins or polysaccharides, that have multiple antigenic determinants (epitopes) that can bind to different antibodies or T cell receptors. Examples of immunogens include bacterial or viral antigens, foreign proteins, and some vaccines.
- Haptens/Incomplete antigens: These are antigens that cannot elicit an immune response by themselves, but only when they are attached to a larger carrier molecule that acts as an immunogen. They are usually small and simple molecules, such as drugs, hormones, or toxins, that have only one or a few antigenic determinants. Examples of haptens include penicillin, urushiol (the allergen in poison ivy), and dinitrophenol.
- Superantigens: These are antigens that can activate a large number of T cells in a nonspecific manner, bypassing the normal antigen processing and presentation pathways. They do so by binding to both the major histocompatibility complex (MHC) class II molecules on antigen-presenting cells (APCs) and the variable region of the T cell receptor (TCR) on T cells, forming a bridge that stimulates T cell proliferation and cytokine release. Superantigens can cause severe inflammatory reactions and diseases, such as toxic shock syndrome and food poisoning. Examples of superantigens include staphylococcal enterotoxins, streptococcal pyrogenic exotoxins, and some viral proteins.
- Tolerogens: These are antigens that induce a state of immunological tolerance rather than an immune response. Tolerance is the lack of reactivity to an antigen that is normally recognized as foreign by the immune system. It can be achieved by exposing the immune system to an antigen in a certain way or at a certain time that prevents its activation or induces its deletion or regulation. Tolerance is important for preventing autoimmune diseases and transplant rejection. Examples of tolerogens include self-antigens, fetal antigens, and some oral antigens.
These are the main types of antigens based on their immune response. However, it is important to note that the same antigen can behave differently depending on the dose, route, frequency, and context of exposure. Therefore, the classification of antigens is not absolute but rather relative and dynamic.
An immunogen is a type of antigen that can trigger a specific immune response by itself. Immunogens are also called complete antigens because they have both antigenic and immunogenic properties. Antigenicity refers to the ability of a substance to bind to antibodies or T cell receptors, while immunogenicity refers to the ability of a substance to induce an immune response.
Immunogens are usually large and complex molecules, such as proteins, peptides, and polysaccharides. They have a molecular weight of more than 10,000 Daltons and contain multiple epitopes or antigenic determinants . Epitopes are the specific regions on an antigen that are recognized by the immune system. Each epitope can bind to a complementary paratope on an antibody or a T cell receptor.
Immunogens can activate both humoral and cell-mediated immune responses. Humoral immunity involves the production of antibodies by B cells, while cell-mediated immunity involves the activation of T cells. Depending on the type and location of the immunogen, different subsets of B cells and T cells are involved in the recognition and elimination of the immunogen.
Some examples of immunogens are:
- Microbial antigens: These are antigens derived from bacteria, viruses, fungi, protozoa, or parasites that infect the host. They can be either exogenous antigens (present outside the host cells) or endogenous antigens (present inside the host cells). Some examples are bacterial cell wall components, viral capsid proteins, fungal spores, protozoan cysts, and parasitic eggs.
- Vaccines: These are preparations of weakened or killed microorganisms or their components that are administered to induce immunity against a specific disease. They mimic the natural infection and stimulate the production of memory B cells and T cells that can provide long-term protection against the disease. Some examples are measles vaccine, polio vaccine, tetanus toxoid, and hepatitis B surface antigen.
- Allergens: These are antigens that cause allergic reactions in some individuals. They trigger an exaggerated immune response that results in inflammation and tissue damage. Some examples are pollen, dust mites, animal dander, bee venom, and food proteins.
- Transplant antigens: These are antigens present on the surface of donor cells or tissues that are transplanted into a recipient. They can elicit an immune response that leads to rejection of the transplant. Some examples are blood group antigens (A, B, O) and human leukocyte antigens (HLA).
Haptens are small molecules that are not immunogenic by themselves, but can become immunogenic when attached to a larger carrier molecule. Haptens are also called incomplete antigens because they cannot elicit an immune response unless they are coupled with a carrier. Examples of haptens include drugs, hormones, toxins, and some polysaccharides.
Haptens can bind to specific antibodies, but they cannot stimulate the production of those antibodies. To do that, they need to be presented to the immune system by a carrier molecule, which is usually a protein. The carrier molecule provides the necessary molecular size and complexity to activate the antigen-presenting cells (APCs) and the helper T cells. The APCs process the hapten-carrier complex and present it to the helper T cells, which then help the B cells to produce antibodies against the hapten.
The antibodies produced against the hapten can recognize and bind to the hapten alone, even if it is not attached to the carrier. This can lead to some unwanted immune reactions, such as allergies and autoimmune diseases. For example, penicillin is a hapten that can bind to proteins in the body and cause an allergic reaction in some people. Similarly, some self-molecules can act as haptens and trigger an autoimmune response when they bind to foreign proteins.
Haptens are useful for studying the specificity and diversity of the immune system. By attaching different haptens to the same carrier molecule, researchers can generate different antibodies that recognize different parts of the molecule. This can help them understand how the immune system distinguishes between different antigens and how it generates a diverse repertoire of antibodies. Haptens are also used for developing vaccines and immunotherapies for various diseases. By conjugating haptens to antigens that are poorly immunogenic, researchers can enhance their immunogenicity and induce a stronger immune response.
Superantigens (SAgs) are a class of antigens that cause non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release. SAgs are produced by some pathogenic viruses and bacteria most likely as a defense mechanism against the immune system.
Unlike conventional antigens, which bind to the antigen-binding site of the T cell receptor (TCR) and are presented by major histocompatibility complex (MHC) molecules on antigen-presenting cells (APCs), SAgs interact with the variable region of the beta chain (Vβ) of the TCR and the MHC class II molecules on APCs. This interaction results in the activation of a large proportion of T cells (up to 25%) regardless of their antigen specificity, leading to a strong inflammatory response and immunomodulation.
Some examples of SAgs include:
- Staphylococcal enterotoxins (SEs), which cause food poisoning and toxic shock syndrome
- Staphylococcal toxic shock syndrome toxin-1 (TSST-1), which causes toxic shock syndrome
- Staphylococcal exfoliative toxins (ETs), which cause scalded skin syndrome
- Streptococcal pyrogenic exotoxins (SPEs), which cause scarlet fever and streptococcal toxic shock syndrome
- Mycoplasma arthritidis mitogen (MAM), which causes arthritis in mice
The diseases associated with exposure to SAgs are, in part, due to hyperactivation of the immune system and subsequent release of biologically active cytokines by activated T cells. These cytokines include interleukin-1 (IL-1), interleukin-2 (IL-2), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and others. The cytokine storm can cause fever, hypotension, shock, organ failure, and death.
SAgs can also induce immunosuppression by deleting or anergizing specific T cell clones, or by inducing regulatory T cells (Tregs) that suppress the immune response. This can lead to impaired immunity against the pathogen or other infections.
SAgs are potential bioterrorism agents because of their ability to induce severe systemic illness with low doses and high mortality rates. They can also be used as immunomodulators for therapeutic purposes, such as in cancer immunotherapy or autoimmune diseases. However, the use of SAgs is limited by their toxicity and lack of specificity. Therefore, novel strategies to target SAgs or their receptors are being explored to enhance their safety and efficacy.
Autoantigens are antigens that are normally present in the body and are recognized by the immune system as self. They are not immunogenic under normal conditions, but they can trigger an immune response in some situations, such as when they are modified by infection, inflammation, or stress. This can lead to autoimmune diseases, which are disorders where the immune system attacks the body`s own tissues and organs.
Some examples of autoantigens are:
- Nucleic acids: DNA and RNA are the genetic material of cells and viruses. They can become autoantigens when they are released from damaged or dying cells or when they form complexes with proteins. Some autoimmune diseases that involve nucleic acid autoantigens are systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and Sjögren`s syndrome.
- Thyroglobulin: Thyroglobulin is a protein that is produced by the thyroid gland and is involved in the synthesis of thyroid hormones. It can become an autoantigen when it is exposed to iodine or other chemicals that alter its structure. Some autoimmune diseases that involve thyroglobulin autoantigens are Hashimoto`s thyroiditis and Graves` disease.
- Insulin: Insulin is a hormone that is produced by the pancreas and regulates blood glucose levels. It can become an autoantigen when it is recognized by T cells or antibodies that target its structure or function. Some autoimmune diseases that involve insulin autoantigens are type 1 diabetes mellitus and insulin resistance.
- Myelin: Myelin is a fatty substance that surrounds and insulates nerve fibers in the central and peripheral nervous system. It can become an autoantigen when it is damaged by infection, trauma, or toxins. Some autoimmune diseases that involve myelin autoantigens are multiple sclerosis (MS) and Guillain-Barré syndrome.
Autoimmune diseases can be classified into two types based on the mechanism of autoimmunity:
- Type II hypersensitivity: This type of autoimmunity involves antibodies that bind to autoantigens on the surface of cells or tissues and cause their destruction or dysfunction. Examples of type II hypersensitivity diseases are hemolytic anemia, myasthenia gravis, and Goodpasture`s syndrome.
- Type III hypersensitivity: This type of autoimmunity involves immune complexes that form between antibodies and soluble autoantigens in the blood or tissues and cause inflammation and tissue damage. Examples of type III hypersensitivity diseases are SLE, RA, and glomerulonephritis.
Autoimmune diseases can also be classified into two types based on the specificity of autoimmunity:
- Organ-specific: This type of autoimmunity involves autoantigens that are restricted to a specific organ or tissue and cause damage to that organ or tissue only. Examples of organ-specific diseases are type 1 diabetes mellitus, Hashimoto`s thyroiditis, and Addison`s disease.
- Systemic: This type of autoimmunity involves autoantigens that are widely distributed throughout the body and cause damage to multiple organs or tissues. Examples of systemic diseases are SLE, RA, and Sjögren`s syndrome.
The exact causes of autoimmune diseases are not fully understood, but they may involve genetic, environmental, hormonal, and immunological factors. Some possible triggers of autoimmunity are:
- Infections: Some infections can mimic or modify autoantigens and induce cross-reactivity or molecular mimicry between foreign antigens and self antigens. Examples of infections that can trigger autoimmunity are Epstein-Barr virus (EBV), cytomegalovirus (CMV), hepatitis C virus (HCV), Helicobacter pylori, Streptococcus pyogenes, and Borrelia burgdorferi.
- Drugs: Some drugs can alter the structure or function of autoantigens or induce hypersensitivity reactions that involve autoantigens. Examples of drugs that can trigger autoimmunity are penicillin, sulfonamides, hydralazine, procainamide, and interferon-alpha.
- Stress: Stress can affect the hormonal balance and immune regulation in the body and increase the susceptibility to autoimmunity. Examples of stressors that can trigger autoimmunity are physical trauma, emotional trauma, surgery, pregnancy, and menopause.
The diagnosis of autoimmune diseases is based on clinical symptoms, laboratory tests, imaging studies, and biopsy. The treatment of autoimmune diseases is aimed at reducing inflammation, suppressing immune responses, replacing deficient hormones or enzymes, and preventing complications. The treatment options may include anti-inflammatory drugs, immunosuppressive drugs, biologic agents, hormone replacement therapy, enzyme replacement therapy, and stem cell transplantation. The prognosis of autoimmune diseases varies depending on the type, severity, and response to treatment of the disease. Some autoimmune diseases can be cured or controlled, while others can be chronic or fatal.
Alloantigens are antigens that are present in some but not all members of the same species. They are also called allogeneic antigens or isoantigens. Alloantigens can elicit an immune response when transferred from one individual to another of the same species, such as during blood transfusion, organ transplantation, or pregnancy.
The most important alloantigens in humans are the ones that determine the blood groups and the human leukocyte antigen (HLA) system. The blood group antigens are carbohydrates that are attached to proteins or lipids on the surface of red blood cells. The HLA antigens are proteins that are expressed on the surface of most nucleated cells and play a key role in presenting antigens to T cells.
The immune system can recognize alloantigens as foreign and mount an immune response against them. This can lead to various complications such as:
- Hemolytic transfusion reaction: This occurs when the recipient`s antibodies bind to the donor`s red blood cells and cause their lysis. This can result in fever, chills, hemoglobinuria, anemia, and shock.
- Graft rejection: This occurs when the recipient`s T cells attack the donor`s cells in the transplanted organ or tissue. This can result in inflammation, necrosis, and loss of function of the graft.
- Hemolytic disease of the newborn: This occurs when the mother`s antibodies cross the placenta and bind to the fetal red blood cells and cause their lysis. This can result in jaundice, anemia, and kernicterus in the newborn.
To prevent these complications, it is important to match the alloantigens between the donor and the recipient as closely as possible before transfusion or transplantation. This can be done by performing blood typing and cross-matching tests for blood group antigens and tissue typing tests for HLA antigens.
Alloantigens can also have beneficial effects on the immune system. For example, they can stimulate the production of natural killer (NK) cells, which are cytotoxic lymphocytes that can kill virus-infected cells and tumor cells. They can also induce immunological tolerance, which is a state of unresponsiveness to a specific antigen. This can prevent autoimmune diseases and enhance graft survival.
Alloantigens are an important aspect of immunology that have both positive and negative implications for human health. They are involved in various clinical scenarios such as transfusion, transplantation, and pregnancy. Understanding their role and function can help improve the outcomes of these situations.
Heterophile antigens are antigens that are shared or similar among different species, classes, or kingdoms of organisms. They can induce cross-reactive immune responses in different hosts. For example, the Forssman antigen is a glycolipid that is present in the red blood cells of some animals, such as sheep and horses, but not in humans. However, some bacteria and plants also express the Forssman antigen, and humans can produce antibodies against it after exposure to these sources. Another example of heterophile antigens are the blood group antigens A and B, which are also found in some bacteria and plants. These antigens can cause hemolytic transfusion reactions or hemolytic disease of the newborn if there is a mismatch between the donor and the recipient.
Heterophile antigens can also be used as diagnostic tools for certain diseases. For example, the heterophile antibody test is a rapid test for infectious mononucleosis, which is caused by the Epstein-Barr virus (EBV). The test detects antibodies that react with antigens from sheep or horse red blood cells, which are similar to some EBV antigens. Another example is the Paul-Bunnell test, which detects antibodies that react with antigens from bovine red blood cells, which are similar to some antigens from the bacterium Corynebacterium diphtheriae. This test can help diagnose diphtheria or other infections caused by Corynebacterium species.
Heterophile antigens can also be used as vaccines or immunotherapy agents for certain diseases. For example, the Bacillus Calmette-Guérin (BCG) vaccine is a live attenuated strain of Mycobacterium bovis, which is closely related to Mycobacterium tuberculosis, the causative agent of tuberculosis. The BCG vaccine stimulates the immune system to produce antibodies and T cells that can cross-react with M. tuberculosis antigens and protect against infection. Another example is the use of heterophile antibodies to treat cancer. For instance, rituximab is a monoclonal antibody that targets the CD20 antigen, which is expressed on B cells and some lymphomas. Rituximab can bind to and destroy cancerous B cells, while sparing normal B cells that have low levels of CD20 expression.
Heterophile antigens are important for understanding the diversity and evolution of the immune system, as well as for developing novel diagnostic and therapeutic strategies for various diseases.
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