| First Author | Steinshamn S | Year | 1996 |
| Journal | J Immunol | Volume | 157 |
| Issue | 5 | Pages | 2155-9 |
| PubMed ID | 8757341 | Mgi Jnum | J:34894 |
| Mgi Id | MGI:82349 | Doi | 10.4049/jimmunol.157.5.2155 |
| Citation | Steinshamn S, et al. (1996) TNF receptors in murine Candida albicans infection: evidence for an important role of TNF receptor p55 in antifungal defense. J Immunol 157(5):2155-9 |
| abstractText | 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. |
