Premium
Experimental Leishmania major infection in mice: role of IL‐10
Author(s) -
CHATELAIN RENÉ,
MAUZE SMITA,
COFFMAN ROBERT L.
Publication year - 1999
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1046/j.1365-3024.1999.00224.x
Subject(s) - immunology , leishmania major , biology , cytokine , interleukin 4 , immune system , in vitro , endogeny , leishmania , interleukin 10 , disease , medicine , parasite hosting , endocrinology , biochemistry , world wide web , computer science
L. major infection of mice induces polarized Th1 and Th2 responses that are correlated with healing of the infection (Th1) or a fatal disease (Th2). The Th subset specific cytokines, IFNγ and IL‐4, themselves were shown to be important factors for the differentiation into the Th1 and Th2 pathways during infection. We studied the role of the Th2 cytokine IL‐10 during leishmania infection: removal of endogenous IL‐10 by anti‐IL‐10 treatment did not alter the Th2 cytokine pattern in non‐healer mice nor did it modulate DTH reactivity, IgE production or fatal disease progression, but partially blocked the IFNγ inhibiting effect of rIL‐4 in healer mice. During chronic infection similar amounts of IL‐10 were produced in both healer and non‐healer mice. However, at early time‐points during infection IL‐10 production was significantly higher in the non‐healer Th2 responder animals. IL‐10 production in vitro caused significant inhibition of in vitro IFNγ production. In conclusion IL‐10, unlike IL‐4 and IFNγ, does not seem to play a readily detectable role in the Th subset differentiation during L. major infection. However, the high production of IL‐10 early during infection in non‐healer mice and inhibition of leishmania –specific IFNγ production may contribute to drive the immune response towards a Th2 response .