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Cytokines in the differentiation of Th1/Th2 CD4+ subsets in leishmaniasis
Author(s) -
Reiner Steven L.,
Locksley Richard M.
Publication year - 1993
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240530409
Subject(s) - effector , biology , leishmania major , major histocompatibility complex , immunology , microbiology and biotechnology , phenotype , mhc class ii , antigen , leishmania , macrophage , parasite hosting , genetics , gene , in vitro , world wide web , computer science
Leishmania major infect only macrophages in the host, where they reside in endolysosomal compartments into which MHC class II molecules co‐localize. Experimental infection in mice has provided a useful model for the differentiation of Th1 CD4+ effector lymphocytes that are required for the generation of IFN‐γ that activates the macrophage to a microbicidal state. Genetically susceptible BALB/c mice aberrantly activate Th2 CD4+ effector cells that are ineffective in arresting infection. Increasing evidence suggests that, rather than discrete parasite antigens or MHC molecules, cytokines mediate the critical decision in the developmental switch to either the Th1 or Th2 effector phenotype.