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Different epitopes of the LACK protein are recognized by V beta 4 V alpha 8 CD4+ T cells in H-2b and H-2d mice susceptible to Leishmania major.
Microbes and Infection
After inoculation of Leishmania major, a rapid production of IL-4 by LACK-specific CD4+ T cells has been shown to drive Th2 cell development in susceptible mice i.e. BALB/c and C57BL/6 mice rendered susceptible by neutralization of IFN-gamma at the onset of infection. Here, we showed that peptide AA 156-173 induced an early IL-4 mRNA expression not only in BALB/c mice but also in resistant B10.D2 mice when IFN-gamma is neutralized. Epitope mapping of LACK protein demonstrated that peptide containing AA 293-305 induced early IL-4 mRNA transcripts in susceptible H-2b mice i.e. BALB/b and resistant C57BL/6 mice when IFN-gamma is neutralized. Stringently, the early IL-4 response to the H-2d (AA 156-173) or the H-2b (AA 293-305) epitopes occurred in V beta 4 V alpha 8 CD4+ T cells from either H-2d or H-2b susceptible mice, respectively.
Animals, Antigens, Protozoan/immunology, CD4-Positive T-Lymphocytes/immunology, Epitopes/immunology, Female, Gene Expression, Interleukin-4/biosynthesis, Interleukin-4/genetics, Leishmania major/immunology, Leishmaniasis, Cutaneous/immunology, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Protozoan Proteins/immunology, RNA, Messenger/biosynthesis, Receptors, Antigen, T-Cell/immunology, T-Lymphocyte Subsets/immunology, Up-Regulation
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