The resolution of lesions induced by Leishmania major in mice requires a functional Fas (APO-1, CD95) pathway of cytotoxicity
Details
Serval ID
serval:BIB_5AEB16DCD0EC
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
The resolution of lesions induced by Leishmania major in mice requires a functional Fas (APO-1, CD95) pathway of cytotoxicity
Journal
European Journal of Immunology
ISSN
0014-2980 (Print)
Publication state
Published
Issued date
01/1998
Volume
28
Number
1
Pages
237-45
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Jan
Research Support, Non-U.S. Gov't --- Old month value: Jan
Abstract
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.
Keywords
Animals
Antigens, CD95/genetics/*immunology
Apoptosis
CD4-Positive T-Lymphocytes/immunology
Cytotoxicity, Immunologic
Disease Susceptibility
Fas Ligand Protein
Interferon Type II/pharmacology
*Leishmania major
Leishmaniasis, Cutaneous/*immunology/pathology
Macrophages/immunology/parasitology
Membrane Glycoproteins/deficiency/genetics/*immunology
Mice
Mice, Inbred C3H
Mice, Inbred C57BL
Mice, Inbred MRL lpr
Mice, Mutant Strains
Recombinant Proteins/immunology
Wound Healing
Pubmed
Web of science
Create date
24/01/2008 16:18
Last modification date
20/08/2019 15:13