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* Biogen-Idec, Cambridge, MA 01746; and
Department of Medicine, Renal Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115
The development of asthma and other atopic diseases is influenced by cytokines produced by Th2 effector T cells. How effector T cell responses are regulated once these cell populations are established remains unclear. The recently described T cell and airway phenotype regulator locus, containing the T cell, Ig domain, mucin domain (TIM) genes, is genetically associated with Th2 cytokine production and Th2-dependent immune responses. In this study, we report the phenotype of the TIM-2 gene-deficient mouse, and demonstrate exacerbated lung inflammation in an airway atopic response model. Immune responses in the TIM-2-deficient mouse reveal disregulated expression of Th2 cytokines, and adoptive transfer experiments show that the T cell compartment is responsible for the heightened inflammatory phenotype. These studies show that TIM-2 is a novel and critical regulator of effector T cell activity.
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 J.V.B. and T.I. were supported by National Institutes of Health Grants DK-39773, DK-72381, and DK-46267.
2 Address correspondence and reprint requests to Dr. Paul D. Rennert, Biogen Idec, 12 Cambridge Center, Cambridge, MA 01746. E-mail address: paul.rennert{at}biogenidec.com
3 Abbreviations used in this paper: TIM, T cell, Ig domain, mucin domain; BALF, bronchial lavage fluid; DC, dendritic cell; ES, embryonic stem; KLH, keyhole limpet hemocyanin; LN, lymph node; mIL, murine IL; RT, reverse transcriptase.
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