Editing Autoimmunity (section)

== Treatments ==

Treatments for autoimmune disease have traditionally been [[immunosuppression|immunosuppressive]], [[anti-inflammatory]], or [[palliative]].<ref name="scedu" /> Managing inflammation is critical in autoimmune diseases.<ref>{{cite journal | vauthors = Nikoopour E, Schwartz JA, Singh B | title = Therapeutic benefits of regulating inflammation in autoimmunity | journal = Inflammation & Allergy - Drug Targets | volume = 7 | issue = 3 | pages = 203–210 | date = September 2008 | pmid = 18782028 | doi = 10.2174/187152808785748155 }}</ref> Non-immunological therapies, such as hormone replacement in Hashimoto's thyroiditis or Type 1 diabetes mellitus treat outcomes of the autoaggressive response, thus these are palliative treatments.  Dietary manipulation limits the severity of celiac disease.  Steroidal or NSAID treatment limits inflammatory symptoms of many diseases. [[IVIG]] is used for [[Chronic inflammatory demyelinating polyneuropathy|CIDP]] and [[Guillain–Barré syndrome|GBS]]. Specific [[immunomodulator]]y therapies, such as the TNFα antagonists (e.g. [[etanercept]]), the B cell depleting agent [[rituximab]], the anti-IL-6 receptor [[tocilizumab]] and the costimulation blocker [[abatacept]] have been shown to be useful in treating RA.  Some of these immunotherapies may be associated with increased risk of adverse effects, such as susceptibility to infection.

[[Helminthic therapy]] is an experimental approach that involves inoculation of the patient with specific parasitic intestinal [[nematodes]] (helminths). There are currently two closely related treatments available, inoculation with either Necator americanus, commonly known as [[hookworm]]s, or Trichuris Suis Ova, commonly known as Pig Whipworm Eggs.<ref name="Zaccone P, Fehervari Z, Phillips JM, Dunne DW, Cooke A 2006 515–23">{{cite journal | vauthors = Zaccone P, Fehervari Z, Phillips JM, Dunne DW, Cooke A | title = Parasitic worms and inflammatory diseases | journal = Parasite Immunology | volume = 28 | issue = 10 | pages = 515–523 | date = October 2006 | pmid = 16965287 | pmc = 1618732 | doi = 10.1111/j.1365-3024.2006.00879.x }}</ref><ref>{{cite journal | vauthors = Dunne DW, Cooke A | title = A worm's eye view of the immune system: consequences for evolution of human autoimmune disease | journal = Nature Reviews. Immunology | volume = 5 | issue = 5 | pages = 420–426 | date = May 2005 | pmid = 15864275 | doi = 10.1038/nri1601 | s2cid = 24659866 }}</ref><ref>{{cite journal | vauthors = Dittrich AM, Erbacher A, Specht S, Diesner F, Krokowski M, Avagyan A, Stock P, Ahrens B, Hoffmann WH, Hoerauf A, Hamelmann E | display-authors = 6 | title = Helminth infection with Litomosoides sigmodontis induces regulatory T cells and inhibits allergic sensitization, airway inflammation, and hyperreactivity in a murine asthma model | journal = Journal of Immunology | volume = 180 | issue = 3 | pages = 1792–1799 | date = February 2008 | pmid = 18209076 | doi = 10.4049/jimmunol.180.3.1792 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Wohlleben G, Trujillo C, Müller J, Ritze Y, Grunewald S, Tatsch U, Erb KJ | title = Helminth infection modulates the development of allergen-induced airway inflammation | journal = International Immunology | volume = 16 | issue = 4 | pages = 585–596 | date = April 2004 | pmid = 15039389 | doi = 10.1093/intimm/dxh062 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Quinnell RJ, Bethony J, Pritchard DI | title = The immunoepidemiology of human hookworm infection | journal = Parasite Immunology | volume = 26 | issue = 11–12 | pages = 443–454 | year = 2004 | pmid = 15771680 | doi = 10.1111/j.0141-9838.2004.00727.x | s2cid = 32598886 }}</ref>

[[T-cell vaccination]] is also being explored as a possible future therapy for autoimmune disorders.{{citation needed|date=December 2019}}

=== Nutrition and autoimmunity ===

Vitamin D/Sunlight
:*Because most human cells and tissues have receptors for vitamin D, including T and B cells, adequate levels of vitamin D can aid in the regulation of the immune system.<ref name="pmid15585788">{{cite journal | vauthors = Holick MF | title = Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease | journal = The American Journal of Clinical Nutrition | volume = 80 | issue = 6 Suppl | pages = 1678S–1688S | date = December 2004 | pmid = 15585788 | doi = 10.1093/ajcn/80.6.1678S | doi-access = free }}</ref>  Vitamin D plays a role in immune function by acting on&nbsp;[[T cell]]s&nbsp;and&nbsp;[[Natural killer cell|natural killer]]&nbsp;cells.<ref name=":0">{{cite journal | vauthors = Yang CY, Leung PS, Adamopoulos IE, Gershwin ME | title = The implication of vitamin D and autoimmunity: a comprehensive review | journal = Clinical Reviews in Allergy & Immunology | volume = 45 | issue = 2 | pages = 217–226 | date = October 2013 | pmid = 23359064 | pmc = 6047889 | doi = 10.1007/s12016-013-8361-3 }}</ref>&nbsp; Research has demonstrated an association between low serum vitamin D and autoimmune diseases, including&nbsp;[[multiple sclerosis]],&nbsp;[[Diabetes mellitus type 1|type 1 diabetes]], and&nbsp;[[Systemic lupus erythematosus|Systemic Lupus Erythematosus]]&nbsp;(commonly referred to simply as lupus).<ref name=":0" /><ref name=":1">{{cite journal | vauthors = Dankers W, Colin EM, van Hamburg JP, Lubberts E | title = Vitamin D in Autoimmunity: Molecular Mechanisms and Therapeutic Potential | journal = Frontiers in Immunology | volume = 7 | pages = 697 | date = 2017 | pmid = 28163705 | pmc = 5247472 | doi = 10.3389/fimmu.2016.00697 | doi-access = free }}</ref><ref name=":2">{{cite journal | vauthors = Agmon-Levin N, Theodor E, Segal RM, Shoenfeld Y | title = Vitamin D in systemic and organ-specific autoimmune diseases | journal = Clinical Reviews in Allergy & Immunology | volume = 45 | issue = 2 | pages = 256–266 | date = October 2013 | pmid = 23238772 | doi = 10.1007/s12016-012-8342-y | s2cid = 13265245 }}</ref>&nbsp;&nbsp;However, since&nbsp;[[Photosensitivity in humans|photosensitivity]]&nbsp;occurs in lupus, patients are advised to avoid sunlight which may be responsible for vitamin D deficiency seen in this disease.<ref name=":0" /><ref name=":1" /><ref name=":2" />&nbsp;[[Polymorphism (biology)|Polymorphisms]]&nbsp;in the&nbsp;[[Calcitriol receptor|vitamin D receptor]]&nbsp;gene are commonly found in people with autoimmune diseases, giving one potential mechanism for vitamin D's role in autoimmunity.<ref name=":0" /><ref name=":1" />&nbsp;There is mixed evidence on the effect of vitamin D supplementation in type 1 diabetes, lupus, and multiple sclerosis.<ref name=":0" /><ref name=":1" /><ref name=":2" />&nbsp;
Omega-3 Fatty Acids
:*Studies have shown that adequate consumption of omega-3 fatty acids counteracts the effects of arachidonic acids, which contribute to symptoms of autoimmune diseases.  Human and animal trials suggest that omega-3 is an effective [[treatment modality]] for many cases of Rheumatoid Arthritis, Inflammatory Bowel Disease, Asthma, and Psoriasis.<ref name="simopoulos">{{cite journal | vauthors = Simopoulos AP | title = Omega-3 fatty acids in inflammation and autoimmune diseases | journal = Journal of the American College of Nutrition | volume = 21 | issue = 6 | pages = 495–505 | date = December 2002 | pmid = 12480795 | doi = 10.1080/07315724.2002.10719248 | s2cid = 16733569 | author-link = Artemis Simopoulos }}</ref>
:*While major depression is not necessarily an autoimmune disease, some of its physiological symptoms are inflammatory and autoimmune in nature.  Omega-3 may inhibit production of interferon gamma and other cytokines which cause the physiological symptoms of depression.  This may be due to the fact that an imbalance in omega-3 and omega-6 fatty acids, which have opposing effects, is instrumental in the etiology of major depression.<ref name="simopoulos" />
Probiotics/Microflora
:*Various types of bacteria and microflora present in fermented dairy products, especially ''Lactobacillus casei'', have been shown to both stimulate immune response to tumors in mice and to regulate immune function, delaying or preventing the onset of nonobese diabetes.  This is particularly true of the Shirota strain of ''L. casei'' (LcS).  The LcS strain is mainly found in yogurt and similar products in Europe and Japan, and rarely elsewhere.<ref name="pmid17311978">{{cite journal | vauthors = Matsuzaki T, Takagi A, Ikemura H, Matsuguchi T, Yokokura T | title = Intestinal microflora: probiotics and autoimmunity | journal = The Journal of Nutrition | volume = 137 | issue = 3 Suppl 2 | pages = 798S–802S | date = March 2007 | pmid = 17311978 | doi = 10.1093/jn/137.3.798S | doi-access = free }}</ref>
[[Antioxidant]]s
:*It has been theorized that free radicals contribute to the onset of type-1 diabetes in infants and young children, and therefore that the risk could be reduced by high intake of antioxidant substances during pregnancy. However, a study conducted in a hospital in Finland from 1997 to 2002 concluded that there was no statistically significant correlation between antioxidant intake and diabetes risk.<ref name="pmid18689383">{{cite journal | vauthors = Uusitalo L, Kenward MG, Virtanen SM, Uusitalo U, Nevalainen J, Niinistö S, Kronberg-Kippilä C, Ovaskainen ML, Marjamäki L, Simell O, Ilonen J, Veijola R, Knip M | display-authors = 6 | title = Intake of antioxidant vitamins and trace elements during pregnancy and risk of advanced beta cell autoimmunity in the child | journal = The American Journal of Clinical Nutrition | volume = 88 | issue = 2 | pages = 458–464 | date = August 2008 | pmid = 18689383 | doi = 10.1093/ajcn/88.2.458 | doi-access = free }}</ref> This study involved monitoring of food intake through questionnaires, and estimated antioxidant intake on this basis, rather than by exact measurements or use of supplements.