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Leishmania donovani Infection of a Susceptible Host Results in CD4 + T‐Cell Apoptosis and Decreased Th1 Cytokine Production
Author(s) -
DAS G.,
VOHRA H.,
RAO K.,
SAHA B.,
MISHRA G. C.
Publication year - 1999
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1999.00486.x
Subject(s) - leishmania donovani , biology , secretion , leishmania , parasite hosting , host (biology) , cytokine , interferon gamma , visceral leishmaniasis , apoptosis , leishmaniasis , interferon , immunology , immunity , kinetoplastida , immune system , microbiology and biotechnology , virology , protozoal disease , genetics , malaria , biochemistry , world wide web , computer science
The disease visceral leishmaniasis is caused by a protozoan parasite, Leishmania donovani and is characterized by depressed cell‐mediated immunity (CMI) and unhindered parasite growth in a susceptible host. The opposite trend is observed in a resistant host. However, the mechanism of this loss of CMI during the progressive disease is unknown as yet. In this report, we demonstrate that more than 40% of CD4 + T cells from a susceptible host undergo apoptosis resulting in a significant decrease in interleukin (IL)‐2 and interferon (IFN)‐γ secretion, leaving IL‐4 secretion unaffected. These changes are not apparent in the case of CD4 + T cells derived from a resistant host. The data reported here suggest that experimental Leishmania donovani infection leads to selective deletion of the IL‐2 and IFN‐γ‐secreting cells but not Th2‐like cells in a susceptible but not a resistant host.