Contribution of the innate immune system to autoimmune myocarditis: a role for complement.
Myocarditis is a principal cause of heart disease among young adults and is often a precursor of heart failure due to dilated cardiomyopathy. We show here that complement is critical for the induction of experimental autoimmune myocarditis and that it acts through complement receptor type 1 (CR1) and type 2 (CR2). We also found a subset of CD44(hi)CD62L(lo) T cells that expresses CR1 and CR2 and propose that both receptors are involved in the expression of B and T cell activation markers, T cell proliferation and cytokine production. These findings provide a mechanism by which activated complement, a key product of the innate immune response, modulates the induction of an autoimmune disease.
Kaya
Z
Z
Department of Pathology, The Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
Afanasyeva
M
M
Wang
Y
Y
Dohmen
K M
KM
Schlichting
J
J
Tretter
T
T
Fairweather
D
D
Holers
V M
VM
Rose
N R
NR
D000328:Adult; D000818:Animals; D015551:Autoimmunity; D003167:Complement Activation; D003165:Complement System Proteins / Q000276:immunology*; D005260:Female; D006801:Humans; D008213:Lymphocyte Activation; D051379:Mice; D009205:Myocarditis / Q000276:immunology*; D011951:Receptors, Complement / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D011951:Receptors, Complement; D003165:Complement System Proteins