TNF receptors in murine Candida albicans infection: evidence for an important role of TNF receptor p55 in antifungal defense.

S. steinshamn*, M.H.A. Bemelmans, L.J. van Tits, K. Bergh, W.A. Buurman, A. Waage

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

TNF mediates multiple biologic activities through two distinct cell surface receptors, TNFR-p55 and TNFR-p75. TNF plays an important role in nonspecific resistance against the fungus Candida albicans. We used transgenic mice deficient for TNFR-p55 or TNFR-p75 to investigate the role of the TNFR in antifungal defense. Mice deficient for TNFR-p55 have highly impaired ability to clear infection with C. albicans and readily succumb to the infection. Also mice deficient for TNFR-p75 had a significant reduction in their ability to clear the fungus although lethality was not increased. These data demonstrate that TNFR-p55 in particular, but also TNFR-p75, plays a definite role in defense against infection with C. albicans. In NMRI mice, infection with C. albicans resulted in a significant systemic release of soluble (s)TNFR-p75. Cyclophosphamide-induced granulocytopenia led to a reduction of sTNFR-p75 release, whereas levels of bioactive TNF in response to fungal infection were increased. Release of sTNFR-p55 was not affected by induction of granulocytopenia. These observations suggest that granulocytes are a source of sTNFR-p75, possibly contributing to regulation of TNF activity during infection with C. albicans.
Original languageEnglish
Pages (from-to)2155-2159
JournalJournal of Immunology
Volume157
Issue number5
Publication statusPublished - 1 Jan 1996

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