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Interactions between T Cells Responding to Concurrent Mycobacterial and Influenza Infections¹

Dominic O. Co^*,, Laura H. Hogan^*, Jozsef Karman^*, Erika Heninger^*, Shoua Vang^*, Krisna Wells, Yoshihiro Kawaoka and Matyas Sandor^2,*,

^* Department of Pathology and Laboratory Medicine, School of Medicine and Public Health, Program in Cellular and Molecular Biology, and Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706

CD4⁺ T cells are central in mediating granuloma formation and limiting growth and dissemination of mycobacterial infections. To determine whether T cells responding to influenza infection can interact with T cells responding to Mycobacterium bovis bacille Calmette-Guérin (BCG) infection and disrupt granuloma formation, we infected mice containing two monoclonal T cell populations specific for the model Ags pigeon cytochrome c (PCC) and hen egg lysozyme (HEL). These mice were chronically infected with PCC epitope-tagged BCG (PCC-BCG) and acutely infected with HEL epitope-tagged influenza virus (HEL-flu). In these mice, PCC-BCG infection is much more abundant in the liver than the lung, whereas HEL-flu infection is localized to the lung. We observe that both T cells have access to both inflammatory sites, but that PCC-specific T cells dominate the PCC-BCG inflammatory site in the liver, whereas HEL-specific T cells dominate the HEL-flu inflammatory site in the lung. Influenza infection, in the absence of an influenza-specific T cell response, is able to increase the activation state and IFN- secretion of PCC-BCG-specific T cells in the granuloma. Activation of HEL-specific T cells allows them to secrete IFN- and contribute to protection in the granuloma. Ultimately, infection with influenza has little effect on bacterial load, and bacteria do not disseminate. In summary, these data illustrate complex interactions between T cell responses to infectious agents that can affect effector responses to pathogens.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants R01 AI48087, R01 AI/HL46430, and R21 AI054893 (to M.S.).

² Address correspondence and reprint requests to Dr. Matyas Sandor, Department of Pathology and Laboratory Medicine, Medical Sciences Center, Room 5468, University of Wisconsin, 1300 University Avenue, Madison, WI 53706. E-mail address: msandor{at}wisc.edu

³ Abbreviations used in this paper: PCC, pigeon cytochrome c; BCG, bacille Calmette-Guérin; HEL, hen egg lysozyme; BAL, bronchoalveolar lavage; AFB, acid-fast bacilli; Tg, transgenic; wt, wild type.

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