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Article: Corynebacterium parvum- and Mycobacterium bovis Bacillus Calmette-Guérin-Induced Granuloma Formation Is Inhibited in TNF Receptor I (TNF-RI) Knockout Mice and by Treatment with Soluble TNF-RI

TitleCorynebacterium parvum- and Mycobacterium bovis Bacillus Calmette-Guérin-Induced Granuloma Formation Is Inhibited in TNF Receptor I (TNF-RI) Knockout Mice and by Treatment with Soluble TNF-RI
Authors
Senaldi, GiorgioYin, SongmeiShaklee, Christine L.Piguet, Pierre FrançoisMak, Tak W.Ulich, Thomas R.
Issue Date1996
Citation
Journal of Immunology, 1996, v. 157, n. 11, p. 5022-5026 How to Cite?
AbstractThe 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-Guérin (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.
Persistent Identifierhttp://hdl.handle.net/10722/291384
ISSN
0022-1767
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 1.558
ISI Accession Number ID
WOS:A1996VU50100037

 

DC FieldValueLanguage
dc.contributor.authorSenaldi, Giorgio-
dc.contributor.authorYin, Songmei-
dc.contributor.authorShaklee, Christine L.-
dc.contributor.authorPiguet, Pierre François-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorUlich, Thomas R.-
dc.date.accessioned2020-11-17T14:54:15Z-
dc.date.available2020-11-17T14:54:15Z-
dc.date.issued1996-
dc.identifier.citationJournal of Immunology, 1996, v. 157, n. 11, p. 5022-5026-
dc.identifier.issn0022-1767-
dc.identifier.urihttp://hdl.handle.net/10722/291384-
dc.description.abstractThe 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-Guérin (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.-
dc.languageeng-
dc.relation.ispartofJournal of Immunology-
dc.titleCorynebacterium parvum- and Mycobacterium bovis Bacillus Calmette-Guérin-Induced Granuloma Formation Is Inhibited in TNF Receptor I (TNF-RI) Knockout Mice and by Treatment with Soluble TNF-RI-
dc.typeArticle-
dc.identifier.pmid8943410-
dc.identifier.scopuseid_2-s2.0-0030459359-
dc.identifier.volume157-
dc.identifier.issue11-
dc.identifier.spage5022-
dc.identifier.epage5026-
dc.identifier.isiWOS:A1996VU50100037-
dc.identifier.issnl0022-1767-

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