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

Citation
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
Citations number
25
Categorie Soggetti
Immunology
Journal title
The Journal of immunology
ISSN journal
00221767 → ACNP
Volume
157
Issue
11
Year of publication
1996
Pages
5022 - 5026
Database
ISI
SICI code
0022-1767(1996)157:11<5022:CPAMBC>2.0.ZU;2-#
Abstract
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.