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B and T Lymphocyte Attenuator Regulates T Cell Survival in the Lung¹

Christine Deppong^*,, Jessica M. Degnan^*, Theresa L. Murphy, Kenneth M. Murphy^, and Jonathan M. Green^2,*,

^* Departments of Internal Medicine and Pathology and Immunology, Graduate Program in Immunology, and Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110

The initiation, intensity, and duration of T cell-directed inflammatory responses are dependent upon the coordination of both activating and inhibitory signals mediated by specific receptors on the T lymphocyte. The recently described receptor, B and T lymphocyte attenuator (BTLA), has been demonstrated to have an important role in limiting the duration of inflammation in a murine model of allergic asthma. In this study, we have examined the role of BTLA on the proliferation, recruitment, and survival of T cells in response to inhaled allergen. We find that there is decreased cell death in T cells from BTLA-deficient mice, whereas proliferation and recruitment to the lungs are unchanged. Thus, the regulation of cell death through BTLA signaling is a key determinant of the inflammatory response in the lung.

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 in part by Grants HL062683 (to J.M.G.) and U19 AI070489 (to J.M.G. and T.L.M.). C.D. was supported by National Institutes of Health Grant T32 HL07317. K.M.M. was supported by the Howard Hughes Medical Institute.

² Address correspondence and reprint requests to Dr. Jonathan M. Green, Washington University School of Medicine, 660 South Euclid Avenue, Box 8052, St. Louis, MO 63110. E-mail address: jgreen{at}im.wustl.edu

³ Abbreviations used in this paper: BTLA, B and T lymphocyte attenuator; PD-1, programmed death receptor 1; 7-AAD, 7-aminoactinomycin D; BAL, bronchoalveolar lavage; HVEM, herpes virus entry mediator.

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