Editing Immune system (section)

== Disorders of human immunity ==
Failures of host defense occur and fall into three broad categories: immunodeficiencies,{{sfn | Sompayrac | 2019 | pp=120–24}} autoimmunity,{{sfn | Sompayrac | 2019 | pp=114–18}} and hypersensitivities.{{sfn | Sompayrac | 2019 | pp=111–14}}

=== Immunodeficiencies ===
{{further|Immunodeficiency}}
[[Immunodeficiency|Immunodeficiencies]] occur when one or more of the components of the immune system are inactive. The ability of the immune system to respond to pathogens is diminished in both the young and the [[old age|elderly]], with immune responses beginning to decline at around 50 years of age due to [[immunosenescence]].<ref>{{cite journal | vauthors = Aw D, Silva AB, Palmer DB | title = Immunosenescence: emerging challenges for an ageing population | journal = Immunology | volume = 120 | issue = 4 | pages = 435–46 | date = Apr 2007 | pmid = 17313487 | pmc = 2265901 | doi = 10.1111/j.1365-2567.2007.02555.x }}</ref><ref name="nutrition">{{cite journal | vauthors = Chandra RK | title = Nutrition and the immune system: an introduction | journal = The American Journal of Clinical Nutrition | volume = 66 | issue = 2 | pages = 460S–63S | date = Aug 1997 | pmid = 9250133 | doi = 10.1093/ajcn/66.2.460S | doi-access = free }}</ref> In [[developed country|developed countries]], [[obesity]], [[alcohol abuse|alcoholism]], and drug use are common causes of poor immune function, while [[malnutrition]] is the most common cause of immunodeficiency in [[developing country|developing countries]].<ref name="nutrition" /> Diets lacking sufficient protein are associated with impaired cell-mediated immunity, complement activity, phagocyte function, [[immunoglobulin A|IgA]] antibody concentrations, and cytokine production. Additionally, the loss of the [[thymus]] at an early age through [[Mutation|genetic mutation]] or surgical removal results in severe immunodeficiency and a high susceptibility to infection.<ref>{{cite journal | vauthors = Miller JF | title = The discovery of thymus function and of thymus-derived lymphocytes | journal = Immunological Reviews | volume = 185 | issue = 1 | pages = 7–14 | date = Jul 2002 | pmid = 12190917 | doi = 10.1034/j.1600-065X.2002.18502.x | s2cid = 12108587 }}</ref> Immunodeficiencies can also be inherited or '[[Immunodeficiency#Acquired immune deficiency|acquired]]'.{{sfn | Reece | 2011 | p=967}} [[Severe combined immunodeficiency]] is a rare [[genetic disorder]] characterized by the disturbed development of functional T cells and B cells caused by numerous genetic mutations.<ref name="five">{{cite journal |vauthors=Burg M, Gennery AR |title=Educational paper: The expanding clinical and immunological spectrum of severe combined immunodeficiency |journal=Eur J Pediatr |volume= 170 |issue=5 |pages=561–571 |year=2011 |doi=10.1007/s00431-011-1452-3 |pmid=21479529 |pmc=3078321 }}</ref> [[Chronic granulomatous disease]], where [[phagocyte]]s have a reduced ability to destroy pathogens, is an example of an inherited, or [[Primary immunodeficiency|congenital, immunodeficiency]]. [[AIDS]] and some types of [[cancer]] cause acquired immunodeficiency.<ref>{{cite journal | vauthors = Joos L, Tamm M | title = Breakdown of pulmonary host defense in the immunocompromised host: cancer chemotherapy | journal = Proceedings of the American Thoracic Society | volume = 2 | issue = 5 | pages = 445–48 | year = 2005 | pmid = 16322598 | doi = 10.1513/pats.200508-097JS }}</ref><ref>{{cite journal | vauthors = Copeland KF, Heeney JL | title = T helper cell activation and human retroviral pathogenesis | journal = Microbiological Reviews | volume = 60 | issue = 4 | pages = 722–42 | date = Dec 1996 | pmid = 8987361 | pmc = 239461 | doi = 10.1128/MMBR.60.4.722-742.1996 }}</ref>

=== Autoimmunity ===
{{further|Autoimmunity}}
[[File:Rheumatoid_Arthritis.JPG|thumb|Joints of a hand swollen and deformed by [[rheumatoid arthritis]], an autoimmune disorder|alt=See caption]]
Overactive immune responses form the other end of immune dysfunction, particularly the [[autoimmune diseases]]. Here, the immune system fails to properly distinguish between [[Self-protein|self]] and non-self, and attacks part of the body. Under normal circumstances, many T cells and antibodies react with "self" peptides.<ref>{{cite journal | vauthors = Miller JF | s2cid = 32476323 | title = Self-nonself discrimination and tolerance in T and B lymphocytes | journal = Immunologic Research | volume = 12 | issue = 2 | pages = 115–30 | year = 1993 | pmid = 8254222 | doi = 10.1007/BF02918299 }}</ref> One of the functions of specialized cells (located in the [[thymus]] and bone marrow) is to present young lymphocytes with [[Self-protein|self antigens]] produced throughout the body and to eliminate those cells that recognize [[Self-protein|self-antigens]], preventing autoimmunity.<ref name="Sproul" /> Common autoimmune diseases include [[Hashimoto's thyroiditis]],<ref name="NIH2017">{{citation-attribution|1={{cite web|title=Hashimoto's disease|url=https://www.womenshealth.gov/a-z-topics/hashimotos-disease|publisher=Office on Women's Health, U.S. Department of Health and Human Services|access-date=17 July 2017|date=12 June 2017|url-status=live|archive-url=https://web.archive.org/web/20170728031758/https://www.womenshealth.gov/a-z-topics/hashimotos-disease|archive-date=28 July 2017}}}}</ref> [[rheumatoid arthritis]],<ref name="Lancet2016">{{cite journal | vauthors = Smolen JS, Aletaha D, McInnes IB | s2cid = 37973054 | title = Rheumatoid arthritis | journal = Lancet | volume = 388 | issue = 10055 | pages = 2023–2038 | date = October 2016 | pmid = 27156434 | doi = 10.1016/S0140-6736(16)30173-8 | url = http://eprints.gla.ac.uk/131249/1/131249.pdf }}</ref> [[diabetes mellitus type 1]],<ref name="Farhy_2015">{{cite journal | vauthors = Farhy LS, McCall AL | title = Glucagon - the new 'insulin' in the pathophysiology of diabetes | journal = Current Opinion in Clinical Nutrition and Metabolic Care | volume = 18 | issue = 4 | pages = 407–14 | date = July 2015 | pmid = 26049639 | doi = 10.1097/mco.0000000000000192 | s2cid = 19872862 }}</ref> and [[systemic lupus erythematosus]].<ref name=NIH2015>{{cite web|title=Handout on Health: Systemic Lupus Erythematosus|url=http://www.niams.nih.gov/health_info/Lupus/default.asp|website=www.niams.nih.gov|access-date=12 June 2016|date=February 2015|url-status=live|archive-url=https://web.archive.org/web/20160617162703/http://www.niams.nih.gov/Health_Info/Lupus/default.asp|archive-date=17 June 2016}}</ref>

=== Hypersensitivity ===
{{further|Hypersensitivity}}
[[Hypersensitivity]] is an immune response that damages the body's own tissues. It is divided into four classes (Type I&nbsp;– IV) based on the mechanisms involved and the time course of the hypersensitive reaction. Type I hypersensitivity is an immediate or [[anaphylaxis|anaphylactic]] reaction, often associated with allergy. Symptoms can range from mild discomfort to death. Type I hypersensitivity is mediated by [[immunoglobulin E|IgE]], which triggers degranulation of [[mast cell]]s and [[basophil granulocyte|basophils]] when cross-linked by antigen.<ref name="USCH">{{cite web|url=http://www.microbiologybook.org/book/immunol-sta.htm|title=Immunology&nbsp;– Chapter Seventeen: Hypersensitivity States| vauthors = Ghaffar A |year=2006|publisher=University of South Carolina School of Medicine|work=Microbiology and Immunology On-line|access-date=29 May 2016}}</ref>
Type II hypersensitivity occurs when antibodies bind to antigens on the individual's own cells, marking them for destruction. This is also called antibody-dependent (or cytotoxic) hypersensitivity, and is mediated by [[immunoglobulin G|IgG]] and [[immunoglobulin M|IgM]] antibodies.<ref name=USCH /> [[Immune complex]]es (aggregations of antigens, complement proteins, and IgG and IgM antibodies) deposited in various tissues trigger Type III hypersensitivity reactions.<ref name=USCH /> Type IV hypersensitivity (also known as cell-mediated or ''delayed type hypersensitivity'') usually takes between two and three days to develop. Type IV reactions are involved in many autoimmune and infectious diseases, but may also involve [[contact dermatitis]]. These reactions are mediated by [[T cell]]s, [[monocyte]]s, and [[macrophage]]s.<ref name=USCH />

=== Idiopathic inflammation ===
{{further|Immune-mediated inflammatory diseases}}
Inflammation is one of the first responses of the immune system to infection,<ref name=autogenerated2 /> but it can appear without known cause.

Inflammation is produced by [[eicosanoid]]s and [[cytokine]]s, which are released by injured or infected cells. Eicosanoids include [[prostaglandin]]s that produce fever and the [[Vasodilation|dilation of blood vessels]] associated with inflammation, and [[leukotriene]]s that attract certain white blood cells (leukocytes).<ref name=autogenerated4 /><ref name=autogenerated1 /> Common cytokines include [[interleukin]]s that are responsible for communication between white blood cells; [[chemokine]]s that promote [[chemotaxis]]; and [[interferon]]s that have anti-viral effects, such as shutting down [[protein biosynthesis|protein synthesis]] in the host cell.<ref name=autogenerated3 /> [[Growth factor]]s and cytotoxic factors may also be released. These cytokines and other chemicals recruit immune cells to the site of infection and promote healing of any damaged tissue following the removal of pathogens.<ref name=autogenerated5 />