| First Author | Conceição-Silva F | Year | 1998 |
| Journal | Eur J Immunol | Volume | 28 |
| Issue | 1 | Pages | 237-45 |
| PubMed ID | 9485203 | Mgi Jnum | J:45903 |
| Mgi Id | MGI:1196684 | Doi | 10.1002/(SICI)1521-4141(199801)28:01<237::AID-IMMU237>3.0.CO;2-O |
| Citation | Conceicao-Silva F, et al. (1998) The resolution of lesions induced by Leishmania major in mice requires a functional Fas (APO-1, CD95) pathway of cytotoxicity. Eur J Immunol 28(1):237-45 |
| abstractText | Normal or perforin-deficient C57BL/6 mice are able to heal spontaneously cutaneous lesions induced by Leishmania major. In this report, we show that syngeneic gld and lpr mice, lacking a functional Fas system, fail to heal their lesions. This inability to control infection could not be attributed either to a failure to mount a protective CD4+ Th1 response or to an unresponsiveness of their macrophages to the activating signals of IFN-gamma. The observation showing that administration of exogenous recombinant Fas ligand (FasL) to FasL-deficient mice resulted in the resolution of cutaneous lesions demonstrates the importance of the Fas-FasL pathway in the elimination of parasites. Furthermore, macrophages infected with L. major in vitro up-regulate their surface expression of Fas in response to IFN-gamma and as a result become susceptible to CD4+ T cell-induced apoptotic death. These results suggest that the CD4+ T cell-induced apoptotic death of MHC class II-expressing antigen-presenting cells, observed in vitro and operating through the Fas (Apo-1/CD95) pathway, is relevant in vivo. |
