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Here, we investigated whether<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content>activation holds the potential for impacting the severity of experimental autoimmune myasthenia gravis (<jats:styled-content style=\"fixed-case\">EAMG<\/jats:styled-content>) induced following immunization of<jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>ewis rats with the acetylcholine receptor (<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>)<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>97\u2013116 peptide. This report demonstrates reduced<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content>expression by both<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>cells and<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>cells residing in spleen and lymph nodes following<jats:styled-content style=\"fixed-case\">EAMG<\/jats:styled-content>induction.<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content>stimulation inhibited anti\u2010<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>antibody production and proliferation of<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\u2010specific lymphocytes in vitro. Inhibition was blocked with the<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content>antagonists or protein kinase<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>inhibitor. We also determined that the development of<jats:styled-content style=\"fixed-case\">EAMG<\/jats:styled-content>was accompanied by a<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010helper cell imbalance that could be restored following<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content>stimulation that resulted in increased<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>reg cell levels and a reduction in<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1\u2010,<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h2\u2010, and<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h17\u2010cell subtypes. An<jats:styled-content style=\"fixed-case\">EAMG<\/jats:styled-content>\u2010preventive treatment regimen was established that consisted of (2\u2010(p\u2010(2\u2010carbonylethyl)phenylethylamino)\u20105\u2010N\u2010ethylcarboxamidoadenosine) (<jats:styled-content style=\"fixed-case\">CG<\/jats:styled-content>S21680;<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content>agonist) administration 1 day prior to<jats:styled-content style=\"fixed-case\">EAMG<\/jats:styled-content>induction. Administration of<jats:styled-content style=\"fixed-case\">CG<\/jats:styled-content>S21680 29 days post<jats:styled-content style=\"fixed-case\">EAMG<\/jats:styled-content>induction (therapeutic treatment) also ameliorated disease severity. We conclude that<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content>agonists may represent a new class of compounds that can be developed for use in the treatment of myasthenia gravis or other<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell\u2010 and<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>\u2010cell\u2010mediated autoimmune diseases.<\/jats:p>","DOI":"10.1002\/eji.201142088","type":"journal-article","created":{"date-parts":[[2012,4,26]],"date-time":"2012-04-26T18:49:03Z","timestamp":1335466143000},"page":"1140-1151","source":"Crossref","is-referenced-by-count":35,"title":["Activation of the adenosine A2A receptor attenuates experimental autoimmune myasthenia gravis severity"],"prefix":"10.1002","volume":"42","author":[{"given":"Na","family":"Li","sequence":"first","affiliation":[{"name":"Department of Neurobiology Harbin Medical University Provincial 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