DAF/CD55 and Protectin/CD59 modulate adaptive immunity and disease outcome in experimental autoimmune myasthenia gravis.
The role of regulators of complement activity (RCA) involving CD55 and CD59 in the pathogenesis of experimental autoimmune myasthenia gravis (EAMG) remains unclear. CD55 and CD59 restrict complement activation by inhibiting C3/C5 convertases' activities and membrane attack complex formation, respectively. Actively immunized EAMG mice deficient in either CD55 or CD59 showed significant differences in adaptive immune responses and worsened disease outcome associated with increased levels of serum cytokines, modified production of acetylcholine receptor antibodies, and more complement deposition at the neuromuscular junction. We conclude that modulation of complement activity by RCA represents an alternative in controlling of autoimmune processes in EAMG.
Department of Neurology & Psychiatry, Saint Louis University School of Medicine, Saint Louis, MO 63104, United States. jsoltys@slu.edu
Jindrich
J
Soltys
Jose A
JA
Halperin
Qin
Q
Xuebin
D056704:Adaptive Immunity; D000818:Animals; D018958:CD55 Antigens / Q000235:genetics / Q000276:immunology*; D018957:CD59 Antigens / Q000235:genetics / Q000276:immunology*; D003165:Complement System Proteins / Q000276:immunology; D016207:Cytokines / Q000097:blood / Q000276:immunology; D004195:Disease Models, Animal; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D020720:Myasthenia Gravis, Autoimmune, Experimental / Q000276:immunology*; D009469:Neuromuscular Junction / Q000276:immunology; D011950:Receptors, Cholinergic / Q000276:immunology
D018958:CD55 Antigens; D018957:CD59 Antigens; D016207:Cytokines; D011950:Receptors, Cholinergic; D003165:Complement System Proteins