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Their intrinsic effector\u2010memory phenotype, enabling secretion of pro\u2010inflammatory cytokines, and their relative abundance in humans imply a significant potential to contribute to autoimmune processes. However, as\n                    <jats:styled-content style=\"fixed-case\">MAIT<\/jats:styled-content>\n                    cells were unknown until recently and specific immunological tools were unavailable, little is known of their roles in disease. Here I review observations from clinical studies and animal models of autoimmune and immune\u2010mediated diseases including the roles of\n                    <jats:styled-content style=\"fixed-case\">MAIT<\/jats:styled-content>\n                    cells in systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease and airways diseases.\n                    <jats:styled-content style=\"fixed-case\">MAIT<\/jats:styled-content>\n                    cell deficiencies are frequently observed in peripheral blood, and at sites of disease such as the airways in asthma. However,\n                    <jats:styled-content style=\"fixed-case\">MAIT<\/jats:styled-content>\n                    cells have a specific sensitivity to suppression by therapeutic corticosteroids that may confound many of these observations, as may the tendency of the surface marker\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    161 to activation\u2010induced down\u2010regulation. Nonetheless, the dependence on bacteria for the development of\n                    <jats:styled-content style=\"fixed-case\">MAIT<\/jats:styled-content>\n                    cells suggests a potentially important protective role linking the influences of early life microbial exposures and subsequent development of autoimmunity. Conversely,\n                    <jats:styled-content style=\"fixed-case\">MAIT<\/jats:styled-content>\n                    cells could contribute to chronic inflammation either through\n                    <jats:styled-content style=\"fixed-case\">TCR<\/jats:styled-content>\n                    \u2010independent activation, or potentially by\n                    <jats:styled-content style=\"fixed-case\">TCR<\/jats:styled-content>\n                    recognition of as yet undiscovered ligands. Future research will be greatly facilitated by the immunological tools that are now available, including murine genetic models and human and murine specific tetramers.\n                  <\/jats:p>","DOI":"10.1111\/imm.12582","type":"journal-article","created":{"date-parts":[[2016,1,18]],"date-time":"2016-01-18T05:34:20Z","timestamp":1453095260000},"page":"1-12","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":113,"title":["Mucosal\u2010associated invariant\n                    <scp>T<\/scp>\n                    cells in autoimmunity, immune\u2010mediated diseases and airways disease"],"prefix":"10.1111","volume":"148","author":[{"given":"Timothy S. C.","family":"Hinks","sequence":"first","affiliation":[{"name":"Department for Microbiology and Immunology The Peter Doherty Institute for Infection and Immunity University of Melbourne Melbourne Victoria Australia"},{"name":"Clinical and Experimental Sciences University of Southampton Faculty of Medicine Sir Henry Wellcome Laboratories Southampton University Hospital Southampton UK"},{"name":"NIHR Southampton Respiratory Biomedical Research Unit Southampton University Hospital Southampton UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,2,9]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1084\/jem.189.12.1907"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature01433"},{"key":"e_1_2_7_4_1","first-page":"3750","volume-title":"Encyclopedia of Immunobiology","author":"Hinks 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