Abstract
Using multimers of MHC class II molecules linked to a peptide derived from the Leishmania LACK antigen, we have compared the fate of parasite-specific CD4+ T cells in resistant and susceptible mice transgenic for the beta chain of a LACK-specific TCR. Activated T cells were readily detected in the draining lymph nodes of infected animals. Although the kinetics of activation and expansion were similar in both strains, T cells from susceptible and resistant mice expressed low- and high-affinity TCR, respectively. As T cells from resistant mice produced more IFN-gamma and less IL-4 than those from susceptible animals, our results suggest that differences in TCR usage between MHC-matched animals may influence the development of the antiparasite immune response.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Animals
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Antigens, Protozoan / immunology*
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CD4-Positive T-Lymphocytes / immunology*
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Cytokines / metabolism
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Dimerization
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Histocompatibility Antigens Class II / immunology
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Immunity, Innate / immunology
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Kinetics
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Leishmania major / immunology*
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Leishmaniasis, Cutaneous / immunology*
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Lymphocyte Activation / immunology*
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C57BL
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Mice, Transgenic
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Molecular Sequence Data
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Protozoan Proteins / immunology*
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Receptors, Antigen, T-Cell, alpha-beta / genetics
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Receptors, Antigen, T-Cell, alpha-beta / immunology
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Staphylococcal Protein A / metabolism
Substances
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Antigens, Protozoan
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Cytokines
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Histocompatibility Antigens Class II
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I-Ad antigen
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Protozoan Proteins
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Receptors, Antigen, T-Cell, alpha-beta
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Staphylococcal Protein A
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LACK antigen, Leishmania