Role of IL-1 and tumor necrosis factor in coxsackie virus-induced autoimmune myocarditis.
We have previously reported that B10.A (H-2a) mice, which are resistant to the induction of postcoxsackievirus autoimmune myocarditis, become susceptible upon treatment with LPS, IL-1, or TNF. In this study, we show that the development of autoimmune myocarditis is associated with infiltration of the heart by inflammatory cells that secrete the cytokines IL-1 and TNF. Local secretion of these cytokines contributes to increased levels of IL-1 and TNF in the serum. Thus, local production of cytokines promotes the induction of this postinfectious autoimmune disease.
Lane
J R
JR
Department of Immunology and Infectious Diseases, Johns Hopkins Medical Institutions, Baltimore, MD 21205.
Neumann
D A
DA
Lafond-Walker
A
A
Herskowitz
A
A
Rose
N R
NR
D000818:Animals; D001323:Autoantibodies / Q000276:immunology; D001327:Autoimmune Diseases / Q000209:etiology*; D003384:Coxsackievirus Infections / Q000150:complications*; D016207:Cytokines / Q000502:physiology; D004770:Enterovirus / Q000472:pathogenicity*; D007074:Immunoglobulin G / Q000276:immunology; D007375:Interleukin-1 / Q000502:physiology*; D007962:Leukocytes / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D008815:Mice, Inbred Strains; D009205:Myocarditis / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D009210:Myofibrils / Q000276:immunology; D012508:Sarcolemma / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D001323:Autoantibodies; D016207:Cytokines; D007074:Immunoglobulin G; D007375:Interleukin-1; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha