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The Journal of Immunology, 2001, 167: 2219-2226.
Copyright © 2001 by The American Association of Immunologists

V{beta}6+ T Cells Are Obligatory for Vaccine-Induced Immunity to Histoplasma capsulatum1

George S. Deepe, Jr.2 and Reta Gibbons

Division of Infectious Diseases, University of Cincinnati College of Medicine, and Veterans Affairs Hospital, Cincinnati, OH 45267

We examined TCR usage to a protective fragment of heat shock protein 60 from the fungus, Histoplasma capsulatum. Nearly 90% of T cell clones from C57BL/6 mice vaccinated with this protein were V{beta}6+; the remainder were V{beta}14+. Amino acid motifs of the CDR3 region from V{beta}6+ cells were predominantly IxGGG, IGG, or SxxGG, whereas it was uniformly SFSGG for V{beta}14+ clones. Short term T cell lines from V{beta}6+-depleted mice failed to recognize Ag, and no T cell clones could be generated. To determine whether V{beta}6+ cells were functionally important, we eliminated them during vaccination. Depletion of V{beta}6+ cells abrogated protection in vivo and upon adoptive transfer of cells into TCR {alpha}{beta}-/- mice. Transfer of a V{beta}6+, but not a V{beta}14+, clone into TCR {alpha}{beta}-/- mice prolonged survival. Cytokine generation by Ag-stimulated splenocytes from immunized mice depleted of V{beta}6+ cells was similar to that of controls. The efficacy of the V{beta}6+ clone was associated with elevated production of IFN-{gamma}, TNF-{alpha}, and GM-CSF compared with that of the V{beta}14+ clone. More V{beta}6+ cells were present in lungs and spleens of TCR {alpha}{beta}-/- on day 3 postinfection compared with V{beta}14+ cells. Thus, a single V{beta} family was essential for vaccine-induced immunity. Moreover, the mechanism by which V{beta}6+ contributed to protective immunity differed between unfractionated splenocytes and T cell clones.




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