{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T12:48:32Z","timestamp":1790340512411,"version":"4.1.0"},"reference-count":39,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2008,6,28]],"date-time":"2008-06-28T00:00:00Z","timestamp":1214611200000},"content-version":"vor","delay-in-days":27,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of the New York Academy of Sciences"],"published-print":{"date-parts":[[2008,6]]},"abstract":"<jats:p>Mice deficient for complement factors C3, C4, or C5 are resistant to experimental autoimmune myasthenia gravis (EAMG). Acetylcholine receptor (AChR) immune lymph node cells (LNC) of C3 deficient mice produce less interleukin 6 (IL\u20106), and EAMG\u2010resistant IL\u20106 deficient mice have less serum C3. Increased serum C1q\u2010circulating immune complex (CIC) levels correlated with EAMG disease severity in RIIIS\/J mice. The CIC promotes EAMG severity by stimulating the production of LNC IL\u20106, serum C1q, and C3 via FC\u03b3R interaction. Therefore, EAMG\/MG could be treated by blocking the activation of classical complement pathway (CCP) and\/or IL\u20106. Anti\u2010C1q antibody administration before and following AChR immunization suppressed EAMG by reducing LNC IL\u20106 production and neuromuscular junction deposits of IgG, C3, and C5b\u2010C9 complexes. Treatment with low dose (10\u2003\u03bcg) of anti\u2010C1q antibody twice a week for 4 weeks in mice with ongoing clinical EAMG reduced the clinical severity of disease and LNC IL\u20106 production. Therefore, inhibitors of CCP factors C1q, C2, or C4 could treat MG and would preserve the alternate complement pathway activation. Our goal is to tailor MG therapy using anti\u2010C2\/C4 reagents in combination, with or without anti\u2010cytokine (e.g., anti\u2010IL\u20106) reagents.<\/jats:p>","DOI":"10.1196\/annals.1405.009","type":"journal-article","created":{"date-parts":[[2008,6,20]],"date-time":"2008-06-20T23:23:28Z","timestamp":1214004208000},"page":"210-219","source":"Crossref","is-referenced-by-count":23,"title":["<i>Classical Complement Pathway in Experimental Autoimmune Myasthenia Gravis Pathogenesis<\/i>"],"prefix":"10.1111","volume":"1132","author":[{"given":"Premkumar","family":"Christadoss","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erdem","family":"T\u00fcz\u00fcn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shamsher S.","family":"Saini","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huan","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2008,6,28]]},"reference":[{"key":"e_1_2_11_2_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0404.2006.00605.x"},{"key":"e_1_2_11_3_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI29894"},{"key":"e_1_2_11_4_2","first-page":"159","article-title":"Myasthenia gravis","volume":"88","author":"Vincent A.","year":"2000","journal-title":"Adv. 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