Targeting Classical Complement Pathway to Treat Complement Mediated Autoimmune Diseases

摘要: Mice deficient for classical complement pathway (CCP) factor C4 are resistant to antibody and mediated experimental autoimmune myasthenia gravis (EAMG). Anti-C1q administration before or following acetylcholine receptor immunization suppresses EAMG development by reducing lymph node cell IL-6 production neuromuscular junction IgG, C3 C5b-C9 deposition. This effect is achieved treating mice with 10 µg of anti-C1q antibody, twice weekly 4 weeks. Treatment a higher amount gives rise increased serum anti-acetylcholine immune complex levels, facilitates kidney IgG deposits thus reduces the treatment efficacy. KO treated display normal system functions intact capacity. Furthermore, CCP inhibition preserves alternative activation, which required host defense against microorganisms. Therefore, might constitute specific approach not only but also other diseases.