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Cytokines in the differentiation of Th1/Th2 CD4+ subsets in leishmaniasis.

作者信息

Reiner S L, Locksley R M

机构信息

Department of Medicine, University of California San Francisco 94143-0654.

出版信息

J Cell Biochem. 1993 Dec;53(4):323-8. doi: 10.1002/jcb.240530409.

DOI:10.1002/jcb.240530409
PMID:7905485
Abstract

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-gamma 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.

摘要

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