{"id":8422,"date":"2025-03-20T13:34:35","date_gmt":"2025-03-20T17:34:35","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathology\/?post_type=chapter&#038;p=8422"},"modified":"2025-08-23T23:53:43","modified_gmt":"2025-08-24T03:53:43","slug":"celiac-disease","status":"publish","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathology\/chapter\/celiac-disease\/","title":{"raw":"Celiac Disease","rendered":"Celiac Disease"},"content":{"raw":"<header class=\"textbox__header\"><\/header>\r\n<div class=\"textbox__content\">\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>Define Celiac disease.<\/li>\r\n \t<li>Describe autoimmune processes underlying Celiac disease.<\/li>\r\n \t<li>Explain how genetic and environmental factors impact on the pathogenesis of Celiac disease.<\/li>\r\n \t<li>Distinguish between Celiac disease and other autoimmune diseases of the gut.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<\/div>\r\n<span style=\"font-family: 'Cormorant Garamond', serif;font-size: 1.602em;font-weight: bold\">Introduction<\/span>\r\n\r\n<\/div>\r\nCeliac disease is a common autoimmune condition, affecting approximately 1 in 100 people worldwide. It is characterized by an [pb_glossary id=\"8508\"]autoimmune response[\/pb_glossary] triggered by consumption of gluten, a protein that is in food products containing wheat, barley, and rye.\r\n<h2>Mechanism<\/h2>\r\nGluten is one of the few chronically consumed proteins that is digested incompletely. Gliadin, a metabolic byproduct of gluten digestion, is bound by secretory [pb_glossary id=\"8905\"]IgA[\/pb_glossary]in the small intestine. Under normal conditions, IgA protects gut [pb_glossary id=\"3805\"]epithelial[\/pb_glossary] cells from pathogens by marking the pathogens for destruction by the immune system. However, in the case of celiac disease, IgA facilitates the transport of gliadin into the [pb_glossary id=\"8907\"]lamina propria [\/pb_glossary]. There, gliadin is deaminated by tissue transglutaminase (ttg). Then, deaminated gliadin is phagocytosed by intestinal [pb_glossary id=\"8462\"]macrophages[\/pb_glossary], broken down into small peptides and presented on [pb_glossary id=\"8477\"]MHC II[\/pb_glossary]. When presented on MHC II, [pb_glossary id=\"8499\"]helper T cells[\/pb_glossary](CD4+ T cells) can bind and be activated by deaminated gliadin epitopes, resulting in the production of inflammatory [pb_glossary id=\"4775\"]cytokines[\/pb_glossary]. The resulting inflammation can damage the epithelium of the small intestine. Simultaneously, [pb_glossary id=\"8475\"]B cells[\/pb_glossary] may be stimulated to produce anti-gliadin IgA and anti-endomysial IgA, or endomysial antibodies (EMAs), which can interfere with the activity of transglutaminase. The cytokines produced by helper (CD4+) T cells can also recruit [pb_glossary id=\"8500\"]cytotoxic (CD8+) T cells[\/pb_glossary]\u00a0, which can worsen epithelial cell damage. As epithelium is destroyed, it becomes possible for more gliadin to enter the lamina propria, propagating the autoimmune process.\r\n<h2>Genetic Predisposition and the Environment<\/h2>\r\nAlthough Celiac disease, like most autoimmune diseases, is influenced by environmental factors there are genes that are associated with the condition. For example, certain alleles of the [pb_glossary id=\"8909\"]human leukocyte antigen[\/pb_glossary] (HLA) gene, which encodes MHC proteins, are common in patients with celiac disease. More specifically, HLA-DQ2 and HLA-DQ8 are risk factors for celiac disease. Interestingly, the extent to which other genes are expressed can influence celiac pathology. For example, the receptor TFR, which is necessary for transporting gliadin complexes across the intestinal epithelium, is overexpressed in people with celiac disease. Numerous environmental factors influence celiac pathology as well, as demonstrated by uneven geographic distribution of the disease, which implies that different lifestyles and climates may impact manifestation. For example, the hygiene hypothesis proposes that decreased exposure to bacterial antigens as an infant may trigger future autoimmunity. In the case of celiacs, the prevalence of [pb_glossary id=\"8910\"]H. pylori[\/pb_glossary]\u00a0is found to be significantly less than the rest of the population. Current data implies that Celiac disease is most prevalent in Europe and Oceania, and least prevalent in South America. While the unequal distribution of celiac disease of ongoing debate, it may be caused by any combination of weather, bacterial populations, hygiene standards, and diet.\r\n\r\n[caption id=\"attachment_8596\" align=\"aligncenter\" width=\"546\"]<img class=\"wp-image-8596 \" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/world_prevalence_text_sharpened.png\" alt=\"Map showing difference in Celiac Disease prevalence across the world\" width=\"546\" height=\"364\" \/> Map showing difference in Celiac Disease prevalence across the world where data is available. \u00a9 Mohammadi et al. is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" rel=\"license\">CC BY (Attribution)<\/a>\u00a0license[\/caption]\r\n<h2>Diagnoses<\/h2>\r\nA non-invasive way to screen for Celiac disease is to perform [pb_glossary id=\"8911\"]serology [\/pb_glossary] to determine titres of anti-gliadin IgA and EMA. However, because anti-gliadin IgA is not uniformly expressed in celiacs or non-celiacs, this test lacks specificity. It can be used as a tool to suggest Celiac disease prevalence or rule out other autoimmune diseases. A definitive diagnosis can be made following [pb_glossary id=\"2375\"]biopsy[\/pb_glossary]\u00a0of the duodenum; the first part of the small intestine. A biopsy of a person with celiac disease would show a damaged duodenum, with destroyed villi, and abnormally long crypts.\r\n\r\n&nbsp;\r\n\r\n[caption id=\"attachment_8581\" align=\"aligncenter\" width=\"875\"]<img class=\" wp-image-8581\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/healthy-vs-celiac-.png\" alt=\"left shows villi of healthy individual. Right shows villi of celiac after exposure to gluten\" width=\"875\" height=\"436\" \/> High magnification samples of intestinal villi with H&amp;E stain from healthy and Celiac patients. Image from: Daley SF &amp; Haseeb M. Celiac Disease. In: StatPearls. Treasure Island (FL): StatPearls Publishing. <span class=\"bk_cite_avail\">Available from: <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK441900\/\">https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK441900\/<\/a> (<a href=\"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/\">CC BY-NC-ND 4.0<\/a>)<\/span>[\/caption]\r\n<h2>Symptoms and Treatment<\/h2>\r\n<div>The symptoms of celiac disease vary among children and adults. In children, symptoms include abdominal distension and pain, failure to thrive, and diarrhea. In adults, though symptoms are more variable, they commonly include bloating, chronic diarrhea, joint pain, and fatigue. The current recommendation for celiac disease treatment is following a strict gluten free diet (GFD), which in most cases removes all symptoms. However, due to cross contamination in factories, restaurants, and even the home, it is extremely difficult for Celiacs to avoid gluten exposure completely. This helps to explain the higher-than-normal incidence rates of secondary diseases in celiac patients, even with adherence to a GFD. This is due to increased inflammation associated with gluten exposure, as well as malnutrition due to poor absorption caused by intestinal damage.<\/div>\r\n<h1>Review Questions<\/h1>\r\n[h5p id=\"421\"]\r\n\r\n&nbsp;","rendered":"<header class=\"textbox__header\"><\/header>\n<div class=\"textbox__content\">\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>Define Celiac disease.<\/li>\n<li>Describe autoimmune processes underlying Celiac disease.<\/li>\n<li>Explain how genetic and environmental factors impact on the pathogenesis of Celiac disease.<\/li>\n<li>Distinguish between Celiac disease and other autoimmune diseases of the gut.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<p><span style=\"font-family: 'Cormorant Garamond', serif;font-size: 1.602em;font-weight: bold\">Introduction<\/span><\/p>\n<\/div>\n<p>Celiac disease is a common autoimmune condition, affecting approximately 1 in 100 people worldwide. It is characterized by an <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_8508\">autoimmune response<\/a> triggered by consumption of gluten, a protein that is in food products containing wheat, barley, and rye.<\/p>\n<h2>Mechanism<\/h2>\n<p>Gluten is one of the few chronically consumed proteins that is digested incompletely. Gliadin, a metabolic byproduct of gluten digestion, is bound by secretory <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_8905\">IgA<\/a>in the small intestine. Under normal conditions, IgA protects gut <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_3805\">epithelial<\/a> cells from pathogens by marking the pathogens for destruction by the immune system. However, in the case of celiac disease, IgA facilitates the transport of gliadin into the <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_8907\">lamina propria <\/a>. There, gliadin is deaminated by tissue transglutaminase (ttg). Then, deaminated gliadin is phagocytosed by intestinal <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_8462\">macrophages<\/a>, broken down into small peptides and presented on <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_8477\">MHC II<\/a>. When presented on MHC II, <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_8499\">helper T cells<\/a>(CD4+ T cells) can bind and be activated by deaminated gliadin epitopes, resulting in the production of inflammatory <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_4775\">cytokines<\/a>. The resulting inflammation can damage the epithelium of the small intestine. Simultaneously, <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_8475\">B cells<\/a> may be stimulated to produce anti-gliadin IgA and anti-endomysial IgA, or endomysial antibodies (EMAs), which can interfere with the activity of transglutaminase. The cytokines produced by helper (CD4+) T cells can also recruit <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_8500\">cytotoxic (CD8+) T cells<\/a>\u00a0, which can worsen epithelial cell damage. As epithelium is destroyed, it becomes possible for more gliadin to enter the lamina propria, propagating the autoimmune process.<\/p>\n<h2>Genetic Predisposition and the Environment<\/h2>\n<p>Although Celiac disease, like most autoimmune diseases, is influenced by environmental factors there are genes that are associated with the condition. For example, certain alleles of the <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_8909\">human leukocyte antigen<\/a> (HLA) gene, which encodes MHC proteins, are common in patients with celiac disease. More specifically, HLA-DQ2 and HLA-DQ8 are risk factors for celiac disease. Interestingly, the extent to which other genes are expressed can influence celiac pathology. For example, the receptor TFR, which is necessary for transporting gliadin complexes across the intestinal epithelium, is overexpressed in people with celiac disease. Numerous environmental factors influence celiac pathology as well, as demonstrated by uneven geographic distribution of the disease, which implies that different lifestyles and climates may impact manifestation. For example, the hygiene hypothesis proposes that decreased exposure to bacterial antigens as an infant may trigger future autoimmunity. In the case of celiacs, the prevalence of <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_8910\">H. pylori<\/a>\u00a0is found to be significantly less than the rest of the population. Current data implies that Celiac disease is most prevalent in Europe and Oceania, and least prevalent in South America. While the unequal distribution of celiac disease of ongoing debate, it may be caused by any combination of weather, bacterial populations, hygiene standards, and diet.<\/p>\n<figure id=\"attachment_8596\" aria-describedby=\"caption-attachment-8596\" style=\"width: 546px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-8596\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/world_prevalence_text_sharpened.png\" alt=\"Map showing difference in Celiac Disease prevalence across the world\" width=\"546\" height=\"364\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/world_prevalence_text_sharpened.png 1244w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/world_prevalence_text_sharpened-300x200.png 300w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/world_prevalence_text_sharpened-1024x682.png 1024w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/world_prevalence_text_sharpened-768x511.png 768w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/world_prevalence_text_sharpened-65x43.png 65w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/world_prevalence_text_sharpened-225x150.png 225w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/world_prevalence_text_sharpened-350x233.png 350w\" sizes=\"auto, (max-width: 546px) 100vw, 546px\" \/><figcaption id=\"caption-attachment-8596\" class=\"wp-caption-text\">Map showing difference in Celiac Disease prevalence across the world where data is available. \u00a9 Mohammadi et al. is licensed under a\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\" rel=\"license\">CC BY (Attribution)<\/a>\u00a0license<\/figcaption><\/figure>\n<h2>Diagnoses<\/h2>\n<p>A non-invasive way to screen for Celiac disease is to perform <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_8911\">serology <\/a> to determine titres of anti-gliadin IgA and EMA. However, because anti-gliadin IgA is not uniformly expressed in celiacs or non-celiacs, this test lacks specificity. It can be used as a tool to suggest Celiac disease prevalence or rule out other autoimmune diseases. A definitive diagnosis can be made following <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_8422_2375\">biopsy<\/a>\u00a0of the duodenum; the first part of the small intestine. A biopsy of a person with celiac disease would show a damaged duodenum, with destroyed villi, and abnormally long crypts.<\/p>\n<p>&nbsp;<\/p>\n<figure id=\"attachment_8581\" aria-describedby=\"caption-attachment-8581\" style=\"width: 875px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-8581\" src=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/healthy-vs-celiac-.png\" alt=\"left shows villi of healthy individual. Right shows villi of celiac after exposure to gluten\" width=\"875\" height=\"436\" srcset=\"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/healthy-vs-celiac-.png 1210w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/healthy-vs-celiac--300x150.png 300w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/healthy-vs-celiac--1024x510.png 1024w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/healthy-vs-celiac--768x383.png 768w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/healthy-vs-celiac--65x32.png 65w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/healthy-vs-celiac--225x112.png 225w, https:\/\/pressbooks.bccampus.ca\/pathology\/wp-content\/uploads\/sites\/1260\/2025\/03\/healthy-vs-celiac--350x174.png 350w\" sizes=\"auto, (max-width: 875px) 100vw, 875px\" \/><figcaption id=\"caption-attachment-8581\" class=\"wp-caption-text\">High magnification samples of intestinal villi with H&amp;E stain from healthy and Celiac patients. Image from: Daley SF &amp; Haseeb M. Celiac Disease. In: StatPearls. Treasure Island (FL): StatPearls Publishing. <span class=\"bk_cite_avail\">Available from: <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK441900\/\">https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK441900\/<\/a> (<a href=\"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/\">CC BY-NC-ND 4.0<\/a>)<\/span><\/figcaption><\/figure>\n<h2>Symptoms and Treatment<\/h2>\n<div>The symptoms of celiac disease vary among children and adults. In children, symptoms include abdominal distension and pain, failure to thrive, and diarrhea. In adults, though symptoms are more variable, they commonly include bloating, chronic diarrhea, joint pain, and fatigue. The current recommendation for celiac disease treatment is following a strict gluten free diet (GFD), which in most cases removes all symptoms. However, due to cross contamination in factories, restaurants, and even the home, it is extremely difficult for Celiacs to avoid gluten exposure completely. This helps to explain the higher-than-normal incidence rates of secondary diseases in celiac patients, even with adherence to a GFD. This is due to increased inflammation associated with gluten exposure, as well as malnutrition due to poor absorption caused by intestinal damage.<\/div>\n<h1>Review Questions<\/h1>\n<div id=\"h5p-421\">\n<div class=\"h5p-iframe-wrapper\"><iframe id=\"h5p-iframe-421\" class=\"h5p-iframe\" data-content-id=\"421\" style=\"height:1px\" src=\"about:blank\" frameBorder=\"0\" scrolling=\"no\" title=\"Celiac Disease\"><\/iframe><\/div>\n<\/div>\n<p>&nbsp;<\/p>\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:\/\/www.researchgate.net\/publication\/275667227_The_relationship_between_intestinal_parasites_and_some_immune-mediated_intestinal_conditions\"><a rel=\"cc:attributionURL\" href=\"https:\/\/www.researchgate.net\/publication\/275667227_The_relationship_between_intestinal_parasites_and_some_immune-mediated_intestinal_conditions\" property=\"dc:title\">World Prevalence of Celiac Disease<\/a>  &copy;  Mohammadi et al.    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY (Attribution)<\/a> license<\/li><li about=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK441900\/\"><a rel=\"cc:attributionURL\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK441900\/\" property=\"dc:title\">healthy vs celiac villi<\/a>  &copy;  Sharon F. Daley; Muhammad Haseeb.    is licensed under a  <a rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/\">CC BY-NC-ND (Attribution NonCommercial NoDerivatives)<\/a> license<\/li><\/ul><\/div><div class=\"glossary\"><span class=\"screen-reader-text\" id=\"definition\">definition<\/span><template id=\"term_8422_8508\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_8508\"><div tabindex=\"-1\"><p>inappropriate immune response to host cells or 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_8422_8905\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_8905\"><div tabindex=\"-1\"><p>antibody crucial for mucosal immunity <\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_3805\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_3805\"><div tabindex=\"-1\"><p>The layer of cells that covers all internal and external surfaces of the body<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_8907\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_8907\"><div tabindex=\"-1\"><p>Connective tissue found under the thin layer of surface epithelium covering a mucous membrane <\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_8462\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_8462\"><div tabindex=\"-1\"><p>large phagocytic cell that engulfs foreign particles and pathogens<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_8477\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_8477\"><div tabindex=\"-1\"><p>protein found on the surface of  antigen-presenting cells that signals to immune cells whether the cell is healthy\/normal or is infected\/cancerous; it provides the appropriate template into which antigens can be loaded for recognition by lymphocytes<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_8499\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_8499\"><div tabindex=\"-1\"><p>cell of the adaptive immune system that binds APCs via MHC II molecules and stimulates B cells or secretes cytokines to initiate the immune response<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_4775\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_4775\"><div tabindex=\"-1\"><p>small proteins released by cells; allow for communication between the cells involved in the same type of immune response\/reaction<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_8475\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_8475\"><div tabindex=\"-1\"><p>lymphocytes that mature in the bone marrow and differentiate into antibody-secreting plasma cells<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_8500\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_8500\"><div tabindex=\"-1\"><p>adaptive immune cell that directly kills infected cells via perforin and granzymes, and releases cytokines to enhance the immune response<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_8909\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_8909\"><div tabindex=\"-1\"><p>genes part of the major histocompatibility complex<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_8910\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_8910\"><div tabindex=\"-1\"><p>Gram-negative, flagellated, helical bacterium that may cause stomach infection<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_8911\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_8911\"><div tabindex=\"-1\"><p>Scientific examination or study of blood serum <\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_8422_2375\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_8422_2375\"><div tabindex=\"-1\"><p>Eextraction of sample cells or tissues for examination to determine the presence or extent of a disease. The tissue is examined under a microscope by a pathologist for histological changes<\/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":2432,"menu_order":8,"template":"","meta":{"pb_show_title":"on","pb_short_title":"Celiac Disease","pb_subtitle":"Celiac Disease","pb_authors":["dylanmann","morganalford"],"pb_section_license":""},"chapter-type":[],"contributor":[538,535],"license":[58],"class_list":["post-8422","chapter","type-chapter","status-publish","hentry","contributor-dylanmann","contributor-morganalford","license-all-rights-reserved"],"part":8316,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/8422","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\/2432"}],"version-history":[{"count":25,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/8422\/revisions"}],"predecessor-version":[{"id":9517,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/8422\/revisions\/9517"}],"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\/8422\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/media?parent=8422"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapter-type?post=8422"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/contributor?post=8422"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/license?post=8422"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}