The membrane attack pathway of complement drives pathology in passively induced experimental autoimmune myasthenia gravis in mice

Clinical and Experimental Immunology

Volumn 146, Issue 2, 2006, Pages 294-302

  Morgan, B P ^a   Chamberlain Banoub, J ^a   Neal, J W ^a   Song, W ^b   Mizuno, M ^a   Harris, C L ^a  

^a CARDIFF UNIVERSITY   (United Kingdom)

^b UNIVERSITY OF PENNSYLVANIA   (United States)

Author keywords

Autoimmunity; Complement; Neuroimmunology; Rodent; Transgenic knock out mice

Indexed keywords

CD59 ANTIGEN; CD59A ANTIGEN; COMPLEMENT MEMBRANE ATTACK COMPLEX; NICOTINIC RECEPTOR; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; AUTOIMMUNE DISEASE; CD59A GENE; COMPLEMENT ACTIVATION; COMPLEMENT SYSTEM; CONTROLLED STUDY; DAF1 GENE; DISEASE RESISTANCE; GENE; GENE LOSS; IMMUNOPATHOGENESIS; MOUSE; MYASTHENIA GRAVIS; MYOSITIS; NERVE ENDING; NEUROMUSCULAR DISEASE; NONHUMAN; PARALYSIS; PRIORITY JOURNAL; SYMPTOM; WILD TYPE;

ANIMALS; ANTIBODIES, MONOCLONAL; ANTIGENS, CD55; ANTIGENS, CD59; COMPLEMENT ACTIVATION; COMPLEMENT C3; COMPLEMENT MEMBRANE ATTACK COMPLEX; DISEASE SUSCEPTIBILITY; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MOTOR ENDPLATE; MYASTHENIA GRAVIS, AUTOIMMUNE, EXPERIMENTAL; RECEPTORS, CHOLINERGIC;

EID: 33750072293     PISSN: 00099104     EISSN: 13652249     Source Type: Journal    
DOI: 10.1111/j.1365-2249.2006.03205.x     Document Type: Article

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