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

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Abstract

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

Steinshamn S, Bemelmans MH, van Tits LJ, Bergh K, Buurman WA, Waage A.

Institute of Cancer Research and Molecular Biology, University Medical Center, Trondheim, Norway.

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
Publication statusPublished - 1 Jan 1996

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