Senaldi G, Yin S, Shaklee C L, Piguet P F, Mak T W, Ulich T R
Amgen, Inc., Thousand Oaks, CA 91320.
J Immunol. 1996 Dec 1;157(11):5022-6.
The aim of this study was to examine the role of TNF receptor I (TNF-RI) in the pathogenesis of heat-killed Corynebacterium parvum- and live bacillus Calmette-Guerin (BCG)-induced granulomas. Granuloma formation was analyzed in TNF-RI knockout mice and after treatment with soluble TNF-RI (sTNF-RI). TNF-RI knockout mice injected with C. parvum or BCG developed fewer and smaller granulomas than wild-type control mice. Mice treated with sTNF-RI from days 7 to 13 after injection of C. parvum or BCG developed fewer and smaller granulomas than saline-treated control mice. Established granulomas regressed in rats treated with sTNF-RI from days 10 to 13 after injection of C. parvum. In conclusion, TNF signaling via TNF-RI contributes to the pathogenesis of C. parvum- and BCG-induced granulomas. sTNF-RI inhibits the development of granulomas and can cause the regression of established granulomas.
本研究的目的是探讨肿瘤坏死因子受体I（TNF-RI）在热灭活细小棒状杆菌和活卡介苗（BCG）诱导的肉芽肿发病机制中的作用。在TNF-RI基因敲除小鼠以及用可溶性TNF-RI（sTNF-RI）治疗后，对肉芽肿形成进行了分析。注射细小棒状杆菌或卡介苗的TNF-RI基因敲除小鼠比野生型对照小鼠形成的肉芽肿更少、更小。在注射细小棒状杆菌或卡介苗后第7至13天用sTNF-RI治疗的小鼠比用生理盐水治疗的对照小鼠形成的肉芽肿更少、更小。在注射细小棒状杆菌后第10至13天用sTNF-RI治疗的大鼠中，已形成的肉芽肿消退。总之，通过TNF-RI的TNF信号传导有助于细小棒状杆菌和卡介苗诱导的肉芽肿的发病机制。sTNF-RI抑制肉芽肿的发展，并可导致已形成的肉芽肿消退。
