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The Journal of Immunology, 2001, 166: 2855-2862.
Copyright © 2001 by The American Association of Immunologists

V{beta}6+ and V{beta}4+ T Cells Exert Cooperative Activity in Clearance of Secondary Infection with Histoplasma capsulatum1

Francisco J. Gomez*, Erin O. Woodward{dagger}, Robyn Pilcher-Roberts{dagger}, Reta S. Gibbons{dagger} and George S. Deepe, Jr.2,{dagger}

* Research Division, Veterans Administration Medical Center, Cincinnati, OH 45202; {dagger} Division of Infectious Diseases, University of Cincinnati School of Medicine, Cincinnati, OH 45267

We previously studied the lung V{beta} TCR repertoire of C57BL/6 mice during primary infection with the pathogen Histoplasma capsulatum. We observed a consistent oligoclonal expansion of V{beta}4+ T cells during the peak of infection and early stages of resolution. The V{beta}4+ family played a role in protective immunity against the fungus. Depletion of this subpopulation of T cells hindered optimal clearance of infection from tissues. In this report we analyze the flux of the V{beta} TCR repertoire in the lungs of C57BL/6 mice with reinfection histoplasmosis. We observed a significant increase in V{beta}6+ T cells on days 7, 10, and 14, the peak and early resolution phases of infection. This skewing was preceded by an increased number of memory T cells within V{beta}6+ cells. The VDJ sequences of V{beta}6 chains were oligoclonal during the early stages of the infection, suggesting that the expansion was driven by a small number of Ags. More than 96% of the expanded V{beta}6+ cells were CD4+. Depletion of V{beta}6+ T cells but not V{beta}4+ T cells induced a modest but significant delay in fungal clearance. Simultaneous depletion of V{beta}4+ and V{beta}6+ T cells induced a more pronounced impairment of host resistance. These studies illustrate the dynamic interactions between V{beta} families in the response to microbial challenge.




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