CORYNEBACTERIUM PARVUM-INDUCED AND MYCOBACTERIUM-BOVIS BACILLUS CALMETTE-GUERIN-INDUCED GRANULOMA-FORMATION IS INHIBITED IN TNF RECEPTOR I (TNF-RI) KNOCKOUT MICE AND BY TREATMENT WITH SOLUBLE TNF-RI
G. Senaldi et al., CORYNEBACTERIUM PARVUM-INDUCED AND MYCOBACTERIUM-BOVIS BACILLUS CALMETTE-GUERIN-INDUCED GRANULOMA-FORMATION IS INHIBITED IN TNF RECEPTOR I (TNF-RI) KNOCKOUT MICE AND BY TREATMENT WITH SOLUBLE TNF-RI, The Journal of immunology, 157(11), 1996, pp. 5022-5026
The aim of this study was to examine the role of TNF receptor I (TNF-R
I) in the pathogenesis of beat-killed Corynebacterium parvum- and live
bacillus Calmette-Guerin (BCG)-induced granulomas, Granuloma formatio
n was analysed in TNF-RI knockout mice and after treatment with solubl
e TNF-RI (sTNF-RI). TNF-RI knockout mice injected with C. parvum or EC
G developed fewer and smaller granulomas than wild-type control mice.
Mice treated with sTNF-RI from days 7 to 13 after injection of C. parv
um or BCG developed fewer and smaller granulomas than saline-treated c
ontrol mice, Established granulomas regressed in rats treated with sTN
F-RI from days 1O to 13 after injection of C. parvum. In conclusion, T
NF signaling via TNF-RI contributes to the pathogenesis of C. parvum-
and BCG-induced granulomas. sTNF-RI inhibits the development of granul
omas and can cause the regression of established granulomas.