Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 133, Issue 6, Pages 1533-1540Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/jid.2013.4
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Funding
- Fundacao de Amparo a Pesquisa do Estado da Bahia (FAPESB) e/Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [SUS0025/2009]
- Pronex (FAPESB/CNPq) [738712006]
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES), Brazil
- CNPq Brazil
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A protective or deleterious role of CD8(+)T cells in human cutaneous leishmaniasis (CL) has been debated. The present report explores the participation of CD8(+)T cells in disease pathogenesis as well as in parasite killing. CD8(+)T cells accumulated in CL lesions as suggested by a higher frequency of CD8(+)CD45RO(+)T cells and CD8(+)CLA(+)T cells compared with peripheral blood mononuclear cells. Upon Leishmania braziliensis restimulation, most of the CD8(+)T cells from the lesion expressed cytolytic markers, CD107a and granzyme B. Granzyme B expression in CL lesions positively correlated with lesion size and percentage of TUNEL-positive cells. We also observed a significantly higher percentage of TUNEL-positive cells and granzyme B expression in the biopsies of patients showing a more intense necrotic process. Furthermore, coculture of infected macrophages and CD8(+) T lymphocytes resulted in the release of granzyme B, and the use of granzyme B inhibitor, as well as z-VAD, Fas:Fc, or anti-IFN-gamma, had no effect upon parasite killing. However, coculture of infected macrophages with CD4(+)T cells strongly increased parasite killing, which was completely reversed by anti-IFN-gamma. Our results reveal a dichotomy in human CL: CD8(+) granzyme B+T cells mediate tissue injury, whereas CD4(+)IFN-gamma T+ cells mediate parasite killing.
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