Rapid early onset lymphocyte cell death in mice resistant, but not susceptible to Leishmania major infection |
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Authors: | Julie Desbarats Jeffrey E Stone Lin Lin Zahra F Zakeri Gerald S Davis Linda M Pfeiffer Richard G Titus M Karen Newell |
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Institution: | (1) Department of Medicine, University of Vermont College of Medicine, Burlington, Vermont 05405, USA;(2) Queens College and Graduate Center, Department of Biology, City University of New York, Flushing, New York 11367, USA;(3) Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80523, USA |
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Abstract: | Leishmania major (Lm) infection in mice is a prototypical model for the role of immune deviation in disease resistance. Resistant strains of mice develop a Th1 response to Lm infection, distinguished by secretion of IL-12 and interferon . In contrast, susceptible strains display sustained IL-4 expression characteristic of a Th2 response. However, when mechanisms of cell death are blocked, mice display a susceptible phenotype even in the presence of a strong Th1 response, suggesting that cell death, and not cytokine bias, may be an importnt factor in disease resistance. Here, we investigated this hypothesis by comparing lymphocyte cellularity, cell death and Fas expression in resistant CBA and susceptible BALB/c mice during the course of Lm infection. We found that delayed onset of cell death and late Fas induction correlated with massive lymphocyte accumulation and susceptibility to leishmaniasis, while early cell death and rapid Fas induction occurred in resistant mice. |
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Keywords: | Apoptosis cell death Fas (CD95) Leishmania lymphocytes T cell Th1 Th2 |
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