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=== Rheumatoid arthritis ===
[[Rheumatoid arthritis]] (RA) primarily targets the joints, causing persistent inflammation that results in joint damage and pain. It
=== Psoriasis and
[[Psoriasis]] is a skin condition characterized by the rapid buildup of skin cells, leading to scaling on the skin's surface. Inflammation and redness around the scales is common.<ref name="National Library of Medicine 2019 x804">{{cite web | title=Psoriasis - Psoriatic Arthritis | publisher=National Library of Medicine | date=2019-02-20 | url=https://medlineplus.gov/psoriasis.html | access-date=2023-06-25}}</ref> Some individuals with psoriasis also develop [[psoriatic arthritis]], which causes joint pain, stiffness, and swelling.<ref name="National Library of Medicine 2016 i430">{{cite web | title=Psoriatic Arthritis | publisher=National Library of Medicine | date=2016-08-25 | url=https://medlineplus.gov/psoriaticarthritis.html | access-date=2023-06-25}}</ref>
===Sjögren's syndrome===
[[Sjögren syndrome]] (SjS, SS) is a long-term autoimmune disease that affects the body's moisture-producing glands (lacrimal and salivary),
=== Systemic lupus erythematosus ===
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=== Type 1 diabetes ===
[[Type 1 diabetes]] is a condition resulting from the immune system attacking insulin-producing [[beta cells]] in the [[pancreas]], leading to [[Hyperglycemia|high blood sugar]] levels. Symptoms include increased [[thirst]], [[frequent urination]], and unexplained [[weight loss]]. It
=== Undifferentiated connective tissue disease ===
[[
== Causes ==
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Evidence suggests a strong genetic component in the development of autoimmune diseases.<ref name="Antonelli Ferrari Ragusa Elia 2020 p. 101387">{{cite journal | vauthors = Antonelli A, Ferrari SM, Ragusa F, Elia G, Paparo SR, Ruffilli I, Patrizio A, Giusti C, Gonnella D, Cristaudo A, Foddis R, Shoenfeld Y, Fallahi P | display-authors = 6 | title = Graves' disease: Epidemiology, genetic and environmental risk factors and viruses | journal = Best Practice & Research. Clinical Endocrinology & Metabolism | volume = 34 | issue = 1 | pages = 101387 | date = January 2020 | pmid = 32107168 | doi = 10.1016/j.beem.2020.101387 | publisher = Elsevier BV | s2cid = 211555101 }}</ref> For instance, conditions such as lupus and multiple sclerosis frequently appear in multiple members of the same family, signifying a potential hereditary link. Furthermore, certain genes have been identified that augment the risk of developing specific autoimmune diseases.<ref name="Wang Wang Gershwin 2015 pp. 369–395">{{cite journal | vauthors = Wang L, Wang FS, Gershwin ME | title = Human autoimmune diseases: a comprehensive update | journal = Journal of Internal Medicine | volume = 278 | issue = 4 | pages = 369–395 | date = October 2015 | pmid = 26212387 | doi = 10.1111/joim.12395 | publisher = Wiley | s2cid = 24386085 | doi-access = free }}</ref>
Experimental methods like genome-wide association studies (GWAS) have proven instrumental in pinpointing genetic risk variants potentially responsible for autoimmune diseases. For example, these studies have been used to identify risk variants for diseases such as
In twin studies, autoimmune diseases consistently demonstrate a higher [[Concordance (genetics)|concordance rate]] among identical twins compared with fraternal twins. For instance, the rate in multiple sclerosis is 35% in identical twins compared to 6% in fraternal twins.<ref name="Willer Dyment Risch Sadovnick 2003 pp. 12877–12882">{{cite journal | vauthors = Willer CJ, Dyment DA, Risch NJ, Sadovnick AD, Ebers GC | title = Twin concordance and sibling recurrence rates in multiple sclerosis | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 100 | issue = 22 | pages = 12877–12882 | date = October 2003 | pmid = 14569025 | pmc = 240712 | doi = 10.1073/pnas.1932604100 | doi-access = free | bibcode = 2003PNAS..10012877W }}</ref><ref>{{cite journal |vauthors=Filippi M, Bar-Or A, Piehl F, Preziosa P, Solari A, Vukusic S, Rocca MA |date=November 2018 |title=Multiple sclerosis |journal=Nature Reviews. Disease Primers |volume=4 |issue=1 |pages=43 |doi=10.1038/s41572-018-0041-4 |pmid=30410033 |s2cid=53238233}}</ref>
==== Balancing infection and autoimmunity ====
There is increasing evidence that certain genes selected during evolution offer a balance between susceptibility to infection and the capacity to avoid autoimmune diseases.<ref name="McKinney Lee Jayne Lyons 2015 pp. 612–616">{{cite journal | vauthors = McKinney EF, Lee JC, Jayne DR, Lyons PA, Smith KG | title = T-cell exhaustion, co-stimulation and clinical outcome in autoimmunity and infection | journal = Nature | volume = 523 | issue = 7562 | pages = 612–616 | date = July 2015 | pmid = 26123020 | pmc = 4623162 | doi = 10.1038/nature14468 | publisher = Springer Science and Business Media LLC | bibcode = 2015Natur.523..612M }}</ref> For example, variants in the ERAP2 gene provide some resistance to infection even though they increase the risk of autoimmunity (positive selection). In contrast, variants in the TYK2 gene protect against autoimmune diseases but increase the risk of infection (negative selection). This suggests the benefits of infection resistance may outweigh the risks of autoimmune diseases, particularly given the historically high risk of infection.<ref name="McKinney Lee Jayne Lyons 2015 pp. 612–616"/>
Several experimental methods such as the [[Genome-wide association study|genome-wide association studies]] (GWAS) have been used to identify genetic risk variants that may be responsible<ref>{{cite journal | vauthors = Gregersen PK, Olsson LM | title = Recent advances in the genetics of autoimmune disease | journal = Annual Review of Immunology | volume = 27 | pages = 363–391 | date = 2009 | pmid = 19302045 | pmc = 2992886 | doi = 10.1146/annurev.immunol.021908.132653 }}</ref> for diseases such as
=== Environmental factors ===
A significant number of environmental factors have been implicated in the development and progression of various autoimmune diseases, either directly or as catalysts. Current research suggests that up to seventy percent of autoimmune diseases could be attributed to environmental influences, which encompass an array of elements such as chemicals, infectious agents, dietary habits, and gut dysbiosis. However, a unifying theory that definitively explains the onset of autoimmune diseases remains elusive, emphasizing the complexity and multifaceted nature of these conditions.<ref name="pmid24688790">{{cite journal | vauthors = Vojdani A | title = A Potential Link between Environmental Triggers and Autoimmunity | journal = Autoimmune Diseases | volume = 2014 | pages = 437231 | date = 2014 | pmid = 24688790 | pmc = 3945069 | doi = 10.1155/2014/437231 | doi-access = free }}</ref>
Various environmental triggers are identified, some of which include:
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* Heightened immune reactivity
Chemicals, which are either a part of
[[Ultraviolet]] (UV) radiation has been implicated as a potential causative factor in the development of autoimmune diseases, such as dermatomyositis.<ref name="pmid23658122">{{cite journal | vauthors = Shah M, Targoff IN, Rice MM, Miller FW, Rider LG | title = Brief report: ultraviolet radiation exposure is associated with clinical and autoantibody phenotypes in juvenile myositis | journal = Arthritis and Rheumatism | volume = 65 | issue = 7 | pages = 1934–1941 | date = July 2013 | pmid = 23658122 | pmc = 3727975 | doi = 10.1002/art.37985 }}</ref> Furthermore, exposure to pesticides has been linked with an increased risk of developing rheumatoid arthritis.<ref name="pmid28718769">{{cite journal | vauthors = Meyer A, Sandler DP, Beane Freeman LE, Hofmann JN, Parks CG | title = Pesticide Exposure and Risk of Rheumatoid Arthritis among Licensed Male Pesticide Applicators in the Agricultural Health Study | journal = Environmental Health Perspectives | volume = 125 | issue = 7 | pages = 077010 | date = July 2017 | pmid = 28718769 | pmc = 5744649 | doi = 10.1289/EHP1013 }}</ref> Vitamin D, on the other hand, appears to play a protective role, particularly in older populations, by preventing immune dysfunctions.<ref name="pmid27543618">{{cite journal | vauthors = Meier HC, Sandler DP, Simonsick EM, Parks CG | title = Association between Vitamin D Deficiency and Antinuclear Antibodies in Middle-Aged and Older U.S. Adults | journal = Cancer Epidemiology, Biomarkers & Prevention | volume = 25 | issue = 12 | pages = 1559–1563 | date = December 2016 | pmid = 27543618 | pmc = 5135624 | doi = 10.1158/1055-9965.EPI-16-0339 }}</ref>
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=== Infections ===
Certain viral and bacterial infections have been linked to autoimmune diseases.<ref name="Getts Chastain Terry Miller 2013 pp. 197–209">{{cite journal | vauthors = Getts DR, Chastain EM, Terry RL, Miller SD | title = Virus infection, antiviral immunity, and autoimmunity | journal = Immunological Reviews | volume = 255 | issue = 1 | pages = 197–209 | date = September 2013 | pmid = 23947356 | pmc = 3971377 | doi = 10.1111/imr.12091 | publisher = Wiley }}</ref> For instance, research suggests that the bacterium that causes [[strep throat]], [[Streptococcus pyogenes|''Streptococcus pyogenes'']], might trigger [[rheumatic fever]], an autoimmune response affecting the heart.<ref name="Karthikeyan Guilherme 2018 pp. 161–174">{{cite journal | vauthors = Karthikeyan G, Guilherme L | title = Acute rheumatic fever | journal = Lancet | volume = 392 | issue = 10142 | pages = 161–174 | date = July 2018 | pmid = 30025809 | doi = 10.1016/s0140-6736(18)30999-1 | publisher = Elsevier BV | s2cid = 51702921 }}</ref> Similarly, some studies propose a link between the
=== Dysregulated immune response ===
Another area of interest is the immune system's ability to distinguish between self and non-self, a function that
=== Negative selection and the role of the thymus ===
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=== Molecular mimicry ===
Some infectious agents, like [[Campylobacter jejuni|''Campylobacter jejuni'']], bear antigens that resemble, but are not identical to, the body's self-molecules. This phenomenon, known as [[molecular mimicry]], can lead to cross-reactivity, where the immune response to such infections inadvertently results in the production of antibodies that also react with self-antigens.<ref name="Rojas Restrepo-Jiménez Monsalve Pacheco 2018 pp. 100–123">{{cite journal | vauthors = Rojas M, Restrepo-Jiménez P, Monsalve DM, Pacheco Y, Acosta-Ampudia Y, Ramírez-Santana C, Leung PS, Ansari AA, Gershwin ME, Anaya JM | display-authors = 6 | title = Molecular mimicry and autoimmunity | journal = Journal of Autoimmunity | volume = 95 | pages = 100–123 | date = December 2018 | pmid = 30509385 | doi = 10.1016/j.jaut.2018.10.012 | publisher = Elsevier BV | s2cid = 54500571 | doi-access = free }}</ref> An example of this is [[Guillain–Barré syndrome]], in which antibodies generated in response to a ''C. jejuni'' infection also react with the gangliosides in the myelin sheath of peripheral nerve axons.<ref name="Jasti Selmi Sarmiento-Monroy Vega 2016 pp. 1175–1189">{{cite journal | vauthors = Jasti AK, Selmi C, Sarmiento-Monroy JC, Vega DA, Anaya JM, Gershwin ME | title = Guillain-Barré syndrome: causes, immunopathogenic mechanisms and treatment | journal = Expert Review of Clinical Immunology | volume = 12 | issue = 11 | pages = 1175–1189 | date = November 2016 | pmid = 27292311 | doi = 10.1080/1744666x.2016.1193006 | publisher = Informa UK Limited | hdl-access = free | s2cid = 45391831 | hdl = 2434/424557 }}</ref>
==Diagnosis==
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=== Multidisciplinary approach ===
Given the systemic nature of many autoimmune disorders, a [[multidisciplinary approach]] may be necessary for their diagnosis and management. This can involve rheumatologists, endocrinologists, gastroenterologists, neurologists, dermatologists, and other specialists, depending on the organs or systems affected by the disease.
In summary, the diagnosis of autoimmune disorders is a complex process that requires a thorough evaluation of clinical, laboratory, and imaging data. Due to the diverse nature of these diseases, an individualized approach, often involving multiple specialists, is crucial for an accurate diagnosis.
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* [[Epigenetics of autoimmune disorders]]
* [[List of autoimmune diseases]]
* [[Immune dysregulation]]
== References ==
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