Lane J R, Neumann D A, Lafond-Walker A, Herskowitz A, Rose N R
Department of Immunology and Infectious Diseases, Johns Hopkins Medical Institutions, Baltimore, MD 21205.
J Immunol. 1993 Aug 1;151(3):1682-90.
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.
我们之前曾报道，对柯萨奇病毒后自身免疫性心肌炎诱导具有抗性的B10.A (H-2a)小鼠，在用LPS、IL-1或TNF处理后会变得易感。在本研究中，我们表明自身免疫性心肌炎的发展与分泌细胞因子IL-1和TNF的炎性细胞浸润心脏有关。这些细胞因子的局部分泌导致血清中IL-1和TNF水平升高。因此，细胞因子的局部产生促进了这种感染后自身免疫性疾病的诱导。
