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Infect. Immun. doi:10.1128/IAI.00943-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Virally activated CD8 T cells home to BCG-induced granulomas, but enhance anti-mycobacterial protection only in immunodeficient mice

Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706; Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison WI 53706

^* To whom correspondence should be addressed. Email: msandor{at}wisc.edu.

	Abstract

The effect of secondary infections on CD4 T cell-regulated chronic granulomatous inflammation is not well understood. Here, we have investigated the effect of an acute viral infection on the cellular composition and bacterial protection in Mycobacterium bovis strain bacille Calmette Guérin (BCG)-induced granulomas using an immunocompetent and a partially immunodeficient murine model. Acute LCMV co-infection of C57BL/6 mice led to substantial accumulation of IFN-producing LCMV-specific T cells in liver granulomas and increased local IFN. Despite traffic of activated T cells that resulted in a CD8 T cell dominated granuloma, BCG liver organ load was unaltered from control levels. In OT-1 TCR transgenic mice, OVA immunization or LCMV co-infection of BCG-infected mice induced CD8 T cell dominated granulomas containing large numbers of non-BCG specific activated T cells. The higher baseline BCG organ load in this CD8 TCR transgenic allowed us to demonstrate that OVA immunization and LCMV co-infection increased anti-BCG protection. Bacterial load remained substantially higher than in mice with a more complete TCR repertoire. Overall, this study suggests that peripherally activated CD8 T cells can be recruited to chronic inflammatory sites, but their contribution to protective immunity is limited to conditions of underlying immunodeficiency.