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J. Exp. Med.,
Volume 189, Number 7, April 5, 1999 1111-1120
By
From the * Departments of Medicine, Experimental leishmaniasis offers a well characterized model of T helper type 1 cell (Th1)-mediated control of infection by an intracellular organism. Susceptible BALB/c mice aberrantly develop Th2 cells in response to infection and are unable to control parasite dissemination. The
early CD4+ T cell response in these mice is oligoclonal and reflects the expansion of V
Howard Hughes
Medical Institute, University of California San Francisco, San Francisco, California 94143; § World Health Organization Immunology Research and Training Center, Institute of Biochemistry,
University of Lausanne, Epalinges CH-1066, Switzerland; Cytel Corporation, San Diego,
California 92121; and the ¶ Institute of Molecular and Cellular Pharmacology, University of Nice,
Valbonne 06560, France
4/
V
8-bearing T cells in response to a single epitope from the parasite Leishmania homologue of
mammalian RACK1 (LACK) antigen. Interleukin 4 (IL-4) generated by these cells is believed
to direct the subsequent Th2 response. We used T cells from T cell receptor-transgenic mice
expressing such a V4/V8 receptor to characterize altered peptide ligands with similar affinity
for I-Ad. Such altered ligands failed to activate IL-4 production from transgenic LACK-specific
T cells or following injection into BALB/c mice. Pretreatment of susceptible mice with altered
peptide ligands substantially altered the course of subsequent infection. The ability to confer a
healer phenotype on otherwise susceptible mice using altered peptides that differed by a single
amino acid suggests limited diversity in the endogenous T cell repertoire recognizing this antigen.
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