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Galectin-2 Suppresses Contact Allergy by Inducing Apoptosis in Activated CD8⁺ T Cells¹

Karin Loser^2,*,, Andreas Sturm, Maik Voskort^*, Verena Kupas^*, Sandra Balkow, Matteo Auriemma^*, Carlo Sternemann^*,, Axel U. Dignass^¶, Thomas A. Luger^* and Stefan Beissert^*,

^* Department of Dermatology and Interdisciplinary Center of Clinical Research (IZKF), University of Münster, Münster, Germany; Department of Internal Medicine, Hepatology and Gastroenterology, Charité–Virchow Campus, Berlin, Germany; and Department of Dermatology, University of Mainz, Mainz, Germany; and ^¶ Markus-Hospital, Frankfurt, Germany

Galectins, a family of structurally related β-galactoside-binding proteins, are expressed by various cells of the immune systems and seem to be important for the regulation of immune responses and immune cell homeostasis. Since it has been demonstrated that galectin-2 regulates cell-mediated inflammatory bowel disease and colitis in mice, we intended to investigate the role of galectin-2 in inflammatory cutaneous T cell-mediated immune responses. To address this issue, groups of naive mice were sensitized to the contact allergen 2,4-dinitro-1-fluorobenzene and systemically treated with galectin-2 to analyze the effects of galectin-2 on contact allergy. Here we show that galectin-2 is expressed in murine skin and is up-regulated upon cutaneous inflammation. Interestingly, treatment of mice with galectin-2 significantly reduced the contact allergy response. This effect was long-lasting since rechallenge of galectin-2-treated mice after a 14-day interval still resulted in a decreased ear swelling. We were able to demonstrate that galectin-2 induced a reduction of MHC class I-restricted immune responses in the treated animals, which was mediated by the induction of apoptosis specifically in activated CD8⁺ T cells. Additionally, we report that the galectin-2-binding protein CD29 is up-regulated on the surface of activated CD8⁺ T cells compared with naive CD8⁺ T cells or CD4⁺ T cells, suggesting that increased galectin-2/CD29 signaling might be responsible for the proapoptotic effects of galectin-2 on activated CD8⁺ T cells. Taken together, these data indicate that galectin-2 may represent a novel therapeutic alternative for the treatment of CD8-mediated inflammatory disorders such as contact allergy.

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 the Interdisciplinary Center of Clinical Research (IZKF; Grant Lo2/017/07 to K.L. and S.B.), the German Cancer Society (Grant 107891 to K.L. and S.B.), and the German Research Association (DFG; Grant Lo817/2-1 to K.L.).

² Address correspondence and reprint requests to Dr. Karin Loser, Department of Dermatology, University of Münster, Von-Esmarch-Strasse 58, D-48149 Münster, Germany. E-mail address: loserk{at}uni-muenster.de

³ Abbreviations used in this paper: DNFB, 2,4-dinitro-1-fluorobenzene; tg, transgenic; wt, wild type; Z-VAD, N-benzyloxycarbonyl valine-alanine-aspartate.