{"id":8352,"date":"2015-10-28T15:56:45","date_gmt":"2015-10-28T19:56:45","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathology\/chapter\/23-4-disruptions-in-the-immune-system\/"},"modified":"2025-08-23T23:53:41","modified_gmt":"2025-08-24T03:53:41","slug":"23-4-disruptions-in-the-immune-system","status":"publish","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathology\/chapter\/23-4-disruptions-in-the-immune-system\/","title":{"raw":"Disruptions in the Immune System","rendered":"Disruptions in the Immune System"},"content":{"raw":"<div class=\"section module\" title=\"42.4.\u00a0Disruptions in the Immune System\" xml:lang=\"en\">\r\n<div class=\"textbox textbox--learning-objectives\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\">Learning Objectives<\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\nBy the end of this section, you will be able to:\r\n<ul>\r\n \t<li class=\"listitem\">Describe hypersensitivity.<\/li>\r\n \t<li class=\"listitem\">Define autoimmunity.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<\/div>\r\nA functioning immune system is essential for survival, but even the sophisticated cellular and molecular defenses of the mammalian immune response can be defeated by pathogens at virtually every step. In the competition between immune protection and pathogen evasion, pathogens have the advantage of more rapid evolution because of their shorter generation time and other characteristics. For instance, <span class=\"emphasis\"><em>Streptococcus pneumoniae <\/em><\/span>(bacterium that cause pneumonia and meningitis) surrounds itself with a capsule that inhibits phagocytes from engulfing it and displaying antigens to the adaptive immune system. <span class=\"emphasis\"><em>Staphylococcus aureus<\/em><\/span> (bacterium that can cause skin infections, abscesses, and meningitis) synthesizes a toxin called leukocidin that kills phagocytes after they engulf the bacterium. Other pathogens can also hinder the adaptive immune system. HIV infects T<sub>H<\/sub> cells via their CD4 surface molecules, gradually depleting the number of T<sub>H<\/sub> cells in the body; this inhibits the adaptive immune system\u2019s capacity to generate sufficient responses to infection or tumors. As a result, HIV-infected individuals often suffer from infections that would not cause illness in people with healthy immune systems but which can cause devastating illness to immune-compromised individuals. Maladaptive responses of immune cells and molecules themselves can also disrupt the proper functioning of the entire system, leading to host cell damage that could become fatal.\r\n<div class=\"section\" title=\"Immunodeficiency\">\r\n<div class=\"titlepage\">\r\n<div>\r\n<div>\r\n<h2 id=\"m44831-fs-idp102177584\"><span class=\"cnx-gentext-section cnx-gentext-autogenerated\"><span class=\"cnx-gentext-section cnx-gentext-t\">Immunodeficiency<\/span><\/span><\/h2>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<span id=\"m44831-fs-idp96686640\"> <\/span>Failures, insufficiencies, or delays at any level of the immune response can allow pathogens or tumor cells to gain a foothold and replicate or proliferate to high enough levels that the immune system becomes overwhelmed. [pb_glossary id=\"8523\"]Immunodeficiency[\/pb_glossary] can be acquired as a result of infection with certain pathogens (such as HIV), chemical exposure (including certain medical treatments), malnutrition, or possibly by extreme stress. For instance, radiation exposure can destroy populations of lymphocytes and elevate an individual\u2019s susceptibility to infections and cancer. Dozens of genetic disorders result in immunodeficiencies, including Severe Combined Immunodeficiency (SCID), Bare lymphocyte syndrome, and MHC II deficiencies. Rarely, primary immunodeficiencies that are present from birth may occur. Neutropenia is one form in which the immune system produces a below-average number of neutrophils, the body\u2019s most abundant phagocytes. As a result, bacterial infections may go unrestricted in the blood, causing serious complications.\r\n\r\n<\/div>\r\n<div class=\"section\" title=\"Hypersensitivities\">\r\n<div class=\"titlepage\">\r\n<div>\r\n<div>\r\n<h2 id=\"m44831-fs-idp9634496\"><span class=\"cnx-gentext-section cnx-gentext-autogenerated\"><span class=\"cnx-gentext-section cnx-gentext-t\">Hypersensitivities<\/span><\/span><\/h2>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<span id=\"m44831-fs-idp114134032\"> <\/span>Maladaptive immune responses toward harmless foreign substances or self antigens that occur after tissue sensitization are termed <span id=\"m44831-autoid-cnx2dbk-id1665649\"><\/span>[pb_glossary id=\"8524\"]<span id=\"m44831-autoid-cnx2dbk-id1665649\"> <\/span>hypersensitivities[\/pb_glossary]. The types of hypersensitivities include immediate, delayed, and autoimmune. A large proportion of the population is affected by one or more types of hypersensitivity.\r\n<div class=\"section\" title=\"Allergies\">\r\n<div class=\"titlepage\">\r\n<div>\r\n<div>\r\n<h2 id=\"m44831-fs-idp223765568\"><span class=\"cnx-gentext-section cnx-gentext-autogenerated\"><span class=\"cnx-gentext-section cnx-gentext-t\">Allergies<\/span><\/span><\/h2>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<span id=\"m44831-fs-idp209444384\"> <\/span>The immune reaction that results from immediate hypersensitivities in which an antibody-mediated immune response occurs within minutes of exposure to a harmless antigen is called an [pb_glossary id=\"8525\"]<span id=\"m44831-autoid-cnx2dbk-id1665670\"> <\/span>allergy[\/pb_glossary]. In the United States, 20 percent of the population exhibits symptoms of allergy or asthma, whereas 55 percent test positive against one or more allergens. Upon initial exposure to a potential allergen, an allergic individual synthesizes antibodies of the IgE class via the typical process of APCs presenting processed antigen to TH cells that stimulate B cells to produce IgE. This class of antibodies also mediates the immune response to parasitic worms. The constant domain of the IgE molecules interact with mast cells embedded in connective tissues. This process primes, or sensitizes, the tissue. Upon subsequent exposure to the same allergen, IgE molecules on mast cells bind the antigen via their variable domains and stimulate the mast cell to release the modified amino acids histamine and serotonin; these chemical mediators then recruit eosinophils which mediate allergic responses. The effects of an allergic reaction range from mild symptoms like sneezing and itchy, watery eyes to more severe or even life-threatening reactions involving intensely itchy welts or hives, airway contraction with severe respiratory distress, and plummeting blood pressure. This extreme reaction is known as anaphylactic shock. If not treated with epinephrine to counter the blood pressure and breathing effects, this condition can be fatal.\r\n\r\n&nbsp;\r\n\r\n<\/div>\r\n\r\n[caption id=\"attachment_8350\" align=\"aligncenter\" width=\"544\"]<img class=\"wp-image-8350 size-full\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2015\/10\/Figure_42_04_01.jpg\" alt=\"A two-panel diagram illustrating the mechanism of an allergic reaction. The top panel shows the initial exposure to an antigen (allergen), where IgE antibodies are produced and bind to receptors on a mast cell, priming it. The bottom panel shows a second exposure, where the allergen binds to the IgE on the mast cell, causing it to release inflammatory chemical mediators.\" width=\"544\" height=\"954\" \/> On first exposure to an allergen, an IgE antibody is synthesized by plasma cells in response to a harmless antigen. The IgE molecules bind to mast cells, and on secondary exposure, the mast cells release histamines and other modulators that affect the symptoms of allergy. (credit: modification of work by NIH)[\/caption]\r\n\r\n<span id=\"m44831-fs-idp113443888\"> <\/span>Delayed hypersensitivity is a cell-mediated immune response that takes approximately one to two days after secondary exposure for a maximal reaction to be observed. This type of hypersensitivity involves the T<sub>H<\/sub>1 cytokine-mediated inflammatory response and may manifest as local tissue lesions or contact dermatitis (rash or skin irritation). Delayed hypersensitivity occurs in some individuals in response to contact with certain types of jewelry or cosmetics. Delayed hypersensitivity facilitates the immune response to poison ivy and is also the reason why the skin test for tuberculosis results in a small region of inflammation on individuals who were previously exposed to <span class=\"emphasis\"><em>Mycobacterium tuberculosis<\/em><\/span>. That is also why cortisone is used to treat such responses: it will inhibit cytokine production.\r\n\r\n<\/div>\r\n<div class=\"section\" title=\"Autoimmunity\">\r\n<div class=\"titlepage\">\r\n<div>\r\n<div>\r\n<h2 id=\"m44831-fs-idp170396736\"><span class=\"cnx-gentext-section cnx-gentext-autogenerated\"><span class=\"cnx-gentext-section cnx-gentext-t\">Autoimmunity<\/span><\/span><\/h2>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<span id=\"m44831-fs-idp204853072\"> <\/span><span id=\"m44831-autoid-cnx2dbk-id1657138\"> <\/span>[pb_glossary id=\"8526\"]Autoimmunity[\/pb_glossary]\u00a0is a type of hypersensitivity to self antigens that affects approximately five percent of the population. Most types of autoimmunity involve the humoral immune response. Antibodies that inappropriately mark self components as foreign are termed <span id=\"m44831-autoid-cnx2dbk-id1657143\"><\/span>[pb_glossary id=\"8527\"]<span id=\"m44831-autoid-cnx2dbk-id1657143\"> <\/span>autoantibodies[\/pb_glossary]. Certain autoimmune diseases have a hereditary (genetic) component. The MHC II molecules expressed on the surface of antigen presenting cells such as macrophages are encoded by human leukocyte antigen (HLA) genes. Certain alleles of this gene, namely HLA-DQ2 and HLA-DQ8, are associated with increased incidence of autoimmune disorders.\r\n<div id=\"m44831-fig-ch42_04_02\" class=\"figure\" title=\"Figure\u00a042.27.\u00a0\">\r\n\r\nThere have been simultaneous \"epidemics\" of autoimmune disorders in certain parts of the world, including North America. This has led some to postulate that environmental factors such as diet and lifestyle can also have a profound influence on autoimmunity. For instance, the hygiene hypothesis suggests that reduced exposure to environmental and\/or commensal microbes may be associated with increased risk of autoimmune conditions, though the mechanism by which that occurs remains unclear. Further, individuals who were not fed breastmilk during their infancy are at increased risk of developing some autoimmune conditions that we expand on in the following chapters or elsewhere, including celiac disease and Type I diabetes mellitus.\r\n<h2 class=\"title\">Section Review<\/h2>\r\n<div class=\"section empty\">\r\n<div class=\"section\">\r\n<div class=\"body\">\r\n\r\n<span id=\"m44831-fs-idp63413328\"> <\/span>Immune disruptions may involve insufficient immune responses or inappropriate immune targets. Immunodeficiency increases an individual's susceptibility to infections and cancers. Hypersensitivities are misdirected responses either to harmless foreign particles, as in the case of allergies, or to host factors, as in the case of autoimmunity. Reactions to self components may be the result of molecular mimicry.\r\n<div class=\"textbox exercises\">\r\n<h3>Exercises<\/h3>\r\n<ol>\r\n \t<li>Allergy to pollen is classified as:\r\n<ol>\r\n \t<li>an autoimmune reaction<\/li>\r\n \t<li>immunodeficiency<\/li>\r\n \t<li>delayed hypersensitivity<\/li>\r\n \t<li>immediate hypersensitivity<\/li>\r\n<\/ol>\r\n<\/li>\r\n \t<li><span id=\"m44831-fs-idp102078144\"><span id=\"m44831-fs-idp196907632\">A potential cause of acquired autoimmunity is ________.<\/span><\/span>\r\n<ol>\r\n \t<li>tissue hypersensitivity<\/li>\r\n \t<li>molecular mimicry<\/li>\r\n \t<li>histamine release<\/li>\r\n \t<li>radiation exposure<\/li>\r\n<\/ol>\r\n<\/li>\r\n \t<li>Autoantibodies are probably involved in:\r\n<ol>\r\n \t<li>reactions to poison ivy<\/li>\r\n \t<li>pollen allergies<\/li>\r\n \t<li>systemic lupus erythematosus<\/li>\r\n \t<li>HIV\/AIDS<\/li>\r\n<\/ol>\r\n<\/li>\r\n \t<li>Which of the following diseases is not due to autoimmunity?\r\n<ol>\r\n \t<li>rheumatic fever<\/li>\r\n \t<li>systemic lupus erythematosus<\/li>\r\n \t<li>diabetes mellitus<\/li>\r\n \t<li>HIV\/AIDS<\/li>\r\n<\/ol>\r\n<\/li>\r\n<\/ol>\r\n<strong>Answers<\/strong>\r\n<ol>\r\n \t<li>D<\/li>\r\n \t<li>B<\/li>\r\n \t<li>C<\/li>\r\n \t<li>D<\/li>\r\n<\/ol>\r\n<\/div>\r\n<h1>Adaptation<\/h1>\r\n<span style=\"text-align: initial;font-size: 1em\">This chapter was adapted by Morgan Alford from the following text:<\/span>\r\n\r\n<a href=\"https:\/\/opentextbc.ca\/biology\/part\/chapter-23-the-immune-system\/\">The Immune System<\/a> in <a href=\"https:\/\/opentextbc.ca\/biology\/\">Concepts of Biology, First Canadian Edition<\/a> by Drs. Jane Gair and Charles Molnar is licensed under a <a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">Creative Commons Attribution 4.0 International License<\/a>.\r\n\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<div id=\"id851471\" class=\"glossary\" title=\"Glossary\">\r\n<div class=\"titlepage\"><\/div>\r\n<\/div>","rendered":"<div class=\"section module\" title=\"42.4.\u00a0Disruptions in the Immune System\" xml:lang=\"en\">\n<div class=\"textbox textbox--learning-objectives\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\">Learning Objectives<\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p>By the end of this section, you will be able to:<\/p>\n<ul>\n<li class=\"listitem\">Describe hypersensitivity.<\/li>\n<li class=\"listitem\">Define autoimmunity.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<p>A functioning immune system is essential for survival, but even the sophisticated cellular and molecular defenses of the mammalian immune response can be defeated by pathogens at virtually every step. In the competition between immune protection and pathogen evasion, pathogens have the advantage of more rapid evolution because of their shorter generation time and other characteristics. For instance, <span class=\"emphasis\"><em>Streptococcus pneumoniae <\/em><\/span>(bacterium that cause pneumonia and meningitis) surrounds itself with a capsule that inhibits phagocytes from engulfing it and displaying antigens to the adaptive immune system. <span class=\"emphasis\"><em>Staphylococcus aureus<\/em><\/span> (bacterium that can cause skin infections, abscesses, and meningitis) synthesizes a toxin called leukocidin that kills phagocytes after they engulf the bacterium. Other pathogens can also hinder the adaptive immune system. HIV infects T<sub>H<\/sub> cells via their CD4 surface molecules, gradually depleting the number of T<sub>H<\/sub> cells in the body; this inhibits the adaptive immune system\u2019s capacity to generate sufficient responses to infection or tumors. As a result, HIV-infected individuals often suffer from infections that would not cause illness in people with healthy immune systems but which can cause devastating illness to immune-compromised individuals. Maladaptive responses of immune cells and molecules themselves can also disrupt the proper functioning of the entire system, leading to host cell damage that could become fatal.<\/p>\n<div class=\"section\" title=\"Immunodeficiency\">\n<div class=\"titlepage\">\n<div>\n<div>\n<h2 id=\"m44831-fs-idp102177584\"><span class=\"cnx-gentext-section cnx-gentext-autogenerated\"><span class=\"cnx-gentext-section cnx-gentext-t\">Immunodeficiency<\/span><\/span><\/h2>\n<\/div>\n<\/div>\n<\/div>\n<p><span id=\"m44831-fs-idp96686640\"> <\/span>Failures, insufficiencies, or delays at any level of the immune response can allow pathogens or tumor cells to gain a foothold and replicate or proliferate to high enough levels that the immune system becomes overwhelmed. <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8352_8523\">Immunodeficiency<\/a> can be acquired as a result of infection with certain pathogens (such as HIV), chemical exposure (including certain medical treatments), malnutrition, or possibly by extreme stress. For instance, radiation exposure can destroy populations of lymphocytes and elevate an individual\u2019s susceptibility to infections and cancer. Dozens of genetic disorders result in immunodeficiencies, including Severe Combined Immunodeficiency (SCID), Bare lymphocyte syndrome, and MHC II deficiencies. Rarely, primary immunodeficiencies that are present from birth may occur. Neutropenia is one form in which the immune system produces a below-average number of neutrophils, the body\u2019s most abundant phagocytes. As a result, bacterial infections may go unrestricted in the blood, causing serious complications.<\/p>\n<\/div>\n<div class=\"section\" title=\"Hypersensitivities\">\n<div class=\"titlepage\">\n<div>\n<div>\n<h2 id=\"m44831-fs-idp9634496\"><span class=\"cnx-gentext-section cnx-gentext-autogenerated\"><span class=\"cnx-gentext-section cnx-gentext-t\">Hypersensitivities<\/span><\/span><\/h2>\n<\/div>\n<\/div>\n<\/div>\n<p><span id=\"m44831-fs-idp114134032\"> <\/span>Maladaptive immune responses toward harmless foreign substances or self antigens that occur after tissue sensitization are termed <span id=\"m44831-autoid-cnx2dbk-id1665649\"><\/span><a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8352_8524\"><span id=\"m44831-autoid-cnx2dbk-id1665649\"> <\/span>hypersensitivities<\/a>. The types of hypersensitivities include immediate, delayed, and autoimmune. A large proportion of the population is affected by one or more types of hypersensitivity.<\/p>\n<div class=\"section\" title=\"Allergies\">\n<div class=\"titlepage\">\n<div>\n<div>\n<h2 id=\"m44831-fs-idp223765568\"><span class=\"cnx-gentext-section cnx-gentext-autogenerated\"><span class=\"cnx-gentext-section cnx-gentext-t\">Allergies<\/span><\/span><\/h2>\n<\/div>\n<\/div>\n<\/div>\n<p><span id=\"m44831-fs-idp209444384\"> <\/span>The immune reaction that results from immediate hypersensitivities in which an antibody-mediated immune response occurs within minutes of exposure to a harmless antigen is called an <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8352_8525\"><span id=\"m44831-autoid-cnx2dbk-id1665670\"> <\/span>allergy<\/a>. In the United States, 20 percent of the population exhibits symptoms of allergy or asthma, whereas 55 percent test positive against one or more allergens. Upon initial exposure to a potential allergen, an allergic individual synthesizes antibodies of the IgE class via the typical process of APCs presenting processed antigen to TH cells that stimulate B cells to produce IgE. This class of antibodies also mediates the immune response to parasitic worms. The constant domain of the IgE molecules interact with mast cells embedded in connective tissues. This process primes, or sensitizes, the tissue. Upon subsequent exposure to the same allergen, IgE molecules on mast cells bind the antigen via their variable domains and stimulate the mast cell to release the modified amino acids histamine and serotonin; these chemical mediators then recruit eosinophils which mediate allergic responses. The effects of an allergic reaction range from mild symptoms like sneezing and itchy, watery eyes to more severe or even life-threatening reactions involving intensely itchy welts or hives, airway contraction with severe respiratory distress, and plummeting blood pressure. This extreme reaction is known as anaphylactic shock. If not treated with epinephrine to counter the blood pressure and breathing effects, this condition can be fatal.<\/p>\n<p>&nbsp;<\/p>\n<\/div>\n<figure id=\"attachment_8350\" aria-describedby=\"caption-attachment-8350\" style=\"width: 544px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-8350 size-full\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2015\/10\/Figure_42_04_01.jpg\" alt=\"A two-panel diagram illustrating the mechanism of an allergic reaction. The top panel shows the initial exposure to an antigen (allergen), where IgE antibodies are produced and bind to receptors on a mast cell, priming it. The bottom panel shows a second exposure, where the allergen binds to the IgE on the mast cell, causing it to release inflammatory chemical mediators.\" width=\"544\" height=\"954\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2015\/10\/Figure_42_04_01.jpg 544w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2015\/10\/Figure_42_04_01-171x300.jpg 171w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2015\/10\/Figure_42_04_01-65x114.jpg 65w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2015\/10\/Figure_42_04_01-225x395.jpg 225w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2015\/10\/Figure_42_04_01-350x614.jpg 350w\" sizes=\"auto, (max-width: 544px) 100vw, 544px\" \/><figcaption id=\"caption-attachment-8350\" class=\"wp-caption-text\">On first exposure to an allergen, an IgE antibody is synthesized by plasma cells in response to a harmless antigen. The IgE molecules bind to mast cells, and on secondary exposure, the mast cells release histamines and other modulators that affect the symptoms of allergy. (credit: modification of work by NIH)<\/figcaption><\/figure>\n<p><span id=\"m44831-fs-idp113443888\"> <\/span>Delayed hypersensitivity is a cell-mediated immune response that takes approximately one to two days after secondary exposure for a maximal reaction to be observed. This type of hypersensitivity involves the T<sub>H<\/sub>1 cytokine-mediated inflammatory response and may manifest as local tissue lesions or contact dermatitis (rash or skin irritation). Delayed hypersensitivity occurs in some individuals in response to contact with certain types of jewelry or cosmetics. Delayed hypersensitivity facilitates the immune response to poison ivy and is also the reason why the skin test for tuberculosis results in a small region of inflammation on individuals who were previously exposed to <span class=\"emphasis\"><em>Mycobacterium tuberculosis<\/em><\/span>. That is also why cortisone is used to treat such responses: it will inhibit cytokine production.<\/p>\n<\/div>\n<div class=\"section\" title=\"Autoimmunity\">\n<div class=\"titlepage\">\n<div>\n<div>\n<h2 id=\"m44831-fs-idp170396736\"><span class=\"cnx-gentext-section cnx-gentext-autogenerated\"><span class=\"cnx-gentext-section cnx-gentext-t\">Autoimmunity<\/span><\/span><\/h2>\n<\/div>\n<\/div>\n<\/div>\n<p><span id=\"m44831-fs-idp204853072\"> <\/span><span id=\"m44831-autoid-cnx2dbk-id1657138\"> <\/span><a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8352_8526\">Autoimmunity<\/a>\u00a0is a type of hypersensitivity to self antigens that affects approximately five percent of the population. Most types of autoimmunity involve the humoral immune response. Antibodies that inappropriately mark self components as foreign are termed <span id=\"m44831-autoid-cnx2dbk-id1657143\"><\/span><a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8352_8527\"><span id=\"m44831-autoid-cnx2dbk-id1657143\"> <\/span>autoantibodies<\/a>. Certain autoimmune diseases have a hereditary (genetic) component. The MHC II molecules expressed on the surface of antigen presenting cells such as macrophages are encoded by human leukocyte antigen (HLA) genes. Certain alleles of this gene, namely HLA-DQ2 and HLA-DQ8, are associated with increased incidence of autoimmune disorders.<\/p>\n<div id=\"m44831-fig-ch42_04_02\" class=\"figure\" title=\"Figure\u00a042.27.\u00a0\">\n<p>There have been simultaneous &#8220;epidemics&#8221; of autoimmune disorders in certain parts of the world, including North America. This has led some to postulate that environmental factors such as diet and lifestyle can also have a profound influence on autoimmunity. For instance, the hygiene hypothesis suggests that reduced exposure to environmental and\/or commensal microbes may be associated with increased risk of autoimmune conditions, though the mechanism by which that occurs remains unclear. Further, individuals who were not fed breastmilk during their infancy are at increased risk of developing some autoimmune conditions that we expand on in the following chapters or elsewhere, including celiac disease and Type I diabetes mellitus.<\/p>\n<h2 class=\"title\">Section Review<\/h2>\n<div class=\"section empty\">\n<div class=\"section\">\n<div class=\"body\">\n<p><span id=\"m44831-fs-idp63413328\"> <\/span>Immune disruptions may involve insufficient immune responses or inappropriate immune targets. Immunodeficiency increases an individual&#8217;s susceptibility to infections and cancers. Hypersensitivities are misdirected responses either to harmless foreign particles, as in the case of allergies, or to host factors, as in the case of autoimmunity. Reactions to self components may be the result of molecular mimicry.<\/p>\n<div class=\"textbox exercises\">\n<h3>Exercises<\/h3>\n<ol>\n<li>Allergy to pollen is classified as:\n<ol>\n<li>an autoimmune reaction<\/li>\n<li>immunodeficiency<\/li>\n<li>delayed hypersensitivity<\/li>\n<li>immediate hypersensitivity<\/li>\n<\/ol>\n<\/li>\n<li><span id=\"m44831-fs-idp102078144\"><span id=\"m44831-fs-idp196907632\">A potential cause of acquired autoimmunity is ________.<\/span><\/span>\n<ol>\n<li>tissue hypersensitivity<\/li>\n<li>molecular mimicry<\/li>\n<li>histamine release<\/li>\n<li>radiation exposure<\/li>\n<\/ol>\n<\/li>\n<li>Autoantibodies are probably involved in:\n<ol>\n<li>reactions to poison ivy<\/li>\n<li>pollen allergies<\/li>\n<li>systemic lupus erythematosus<\/li>\n<li>HIV\/AIDS<\/li>\n<\/ol>\n<\/li>\n<li>Which of the following diseases is not due to autoimmunity?\n<ol>\n<li>rheumatic fever<\/li>\n<li>systemic lupus erythematosus<\/li>\n<li>diabetes mellitus<\/li>\n<li>HIV\/AIDS<\/li>\n<\/ol>\n<\/li>\n<\/ol>\n<p><strong>Answers<\/strong><\/p>\n<ol>\n<li>D<\/li>\n<li>B<\/li>\n<li>C<\/li>\n<li>D<\/li>\n<\/ol>\n<\/div>\n<h1>Adaptation<\/h1>\n<p><span style=\"text-align: initial;font-size: 1em\">This chapter was adapted by Morgan Alford from the following text:<\/span><\/p>\n<p><a href=\"https:\/\/opentextbc.ca\/biology\/part\/chapter-23-the-immune-system\/\">The Immune System<\/a> in <a href=\"https:\/\/opentextbc.ca\/biology\/\">Concepts of Biology, First Canadian Edition<\/a> by Drs. Jane Gair and Charles Molnar is licensed under a <a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">Creative Commons Attribution 4.0 International License<\/a>.<\/p>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<div id=\"id851471\" class=\"glossary\" title=\"Glossary\">\n<div class=\"titlepage\"><\/div>\n<\/div>\n<div class=\"media-attributions clear\" prefix:cc=\"http:\/\/creativecommons.org\/ns#\" prefix:dc=\"http:\/\/purl.org\/dc\/terms\/\"><h2>Media Attributions<\/h2><ul><li about=\"https:\/\/opentextbc.ca\/biology\/chapter\/23-4-disruptions-in-the-immune-system\/\"><a rel=\"cc:attributionURL\" href=\"https:\/\/opentextbc.ca\/biology\/chapter\/23-4-disruptions-in-the-immune-system\/\" property=\"dc:title\">Figure_42_04_01<\/a>  &copy;  Charles Molnar and Jane Gair    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY (Attribution)<\/a> license<\/li><\/ul><\/div><div class=\"glossary\"><span class=\"screen-reader-text\" id=\"definition\">definition<\/span><template id=\"term_8352_8523\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8352_8523\"><div tabindex=\"-1\"><p>failure, insufficiency, or delay at any level of the immune system, which may be acquired or inherited<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8352_8524\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8352_8524\"><div tabindex=\"-1\"><p>spectrum of maladaptive immune responses toward harmless foreign particles or self antigens; occurs after tissue sensitization and includes immediate-type (allergy), delayed-type, and autoimmunity<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8352_8525\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8352_8525\"><div tabindex=\"-1\"><p>immune reaction that results from immediate hypersensitivities in which an antibody-mediated immune response occurs within minutes of exposure to a harmless antigen<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8352_8526\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8352_8526\"><div tabindex=\"-1\"><p>class of hypersensitivity reactions to self antigens<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8352_8527\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8352_8527\"><div tabindex=\"-1\"><p>antibody that incorrectly marks \u201cself\u201d components as foreign and stimulates the immune response<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><\/div>","protected":false},"author":2418,"menu_order":7,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["c-molnar","j-gair","morganalford"],"pb_section_license":"cc-by"},"chapter-type":[],"contributor":[536,537,535],"license":[52],"class_list":["post-8352","chapter","type-chapter","status-publish","hentry","contributor-c-molnar","contributor-j-gair","contributor-morganalford","license-cc-by"],"part":8316,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/8352","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/users\/2418"}],"version-history":[{"count":7,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/8352\/revisions"}],"predecessor-version":[{"id":9515,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/8352\/revisions\/9515"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/parts\/8316"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/8352\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/media?parent=8352"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapter-type?post=8352"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/contributor?post=8352"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/license?post=8352"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}