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J. Biol. Chem., Vol. 281, Issue 19, 13525-13532, May 12, 2006

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Human Keratinocytes Acquire Cellular Cytotoxicity under UV-B Irradiation

IMPLICATION OF GRANZYME B AND PERFORIN^*

Hélène Hernandez-Pigeon¹², Christine Jean¹, Alexandra Charruyer, Marie-José Haure, Matthias Titeux, Laure Tonasso, Anne Quillet-Mary, Caroline Baudouin, Marie Charveron, and Guy Laurent^¶

From the INSERM U563, CPTP, Bat B, Pavillon Lefebvre, Place du Dr. Baylac, Centre Hospitalier Universitaire Purpan, BP 3028, 31024 Toulouse cedex 3, France, CERPER, Institut de Recherche Pierre Fabre, Laboratoire de Biologie Cellulaire Cutanée, Toulouse, France, and the ^¶Service d'Hématologie, Centre Hospitalier Universitaire Purpan, 31059 Toulouse, France

Ultraviolet (UV) radiation from the sun is widely considered as a major cause of human skin photoaging and skin cancer. Granzyme B (GrB) and perforin (PFN) are two proteins contained in granules and implicated in one of the mechanisms by which cytotoxic lymphocytes and natural killer cells exert their cytotoxicity against virus-infected, alloreactive, or transformed cells. The distribution of GrB and PFN in the skin has received little attention. However, Berthou and co-workers (Berthou, C., Michel, L., Soulie, A., Jean-Louis, F., Flageul, B., Dubertret, L., Sigaux, F., Zhang, Y., and Sasportes, M. (1997) J. Immunol. 159, 5293-5300) described that, whereas freshly isolated epidermal cells did not express GrB or PFN, keratinocyte growth to confluence was associated with GrB and PFN mRNA and protein synthesis. In this work, we have investigated the possible role of UV-B on GrB and PFN expression in keratinocytes. We found that UV-B induces GrB and PFN expression in these cells through redox-, epidermal growth factor receptor-, and mitogen-activated protein kinase-dependent signaling. Furthermore, under UV irradiation, keratinocytes acquire a significant cytotoxicity, which is GrB and PFN dependent, toward a variety of cellular targets including transformed T-lymphocytes, melanocytes, and keratinocytes. This phenomenon may have important functional consequences in the regulation of skin inflammatory response and in the emergence of cancer skin.

Received for publication, November 28, 2005 , and in revised form, February 22, 2006.

^* 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 Both authors contributed equally to this work.

² To whom correspondence should be addressed. Tel.: 33-5-62-74-45-61; Fax: 33-5-62-74-45-58; E-mail: helene.hernandez{at}toulouse.inserm.fr.

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This article has been cited by other articles:

				C. Jean, A. Blanc, N. Prade-Houdellier, L. Ysebaert, H. Hernandez-Pigeon, T. Al Saati, M.-J. Haure, A.-M.-L. Coluccia, M. Charveron, E. Delabesse, et al. Epidermal Growth Factor Receptor/{beta}-Catenin/T-Cell Factor 4/Matrix Metalloproteinase 1: A New Pathway for Regulating Keratinocyte Invasiveness after UVA Irradiation Cancer Res., April 15, 2009; 69(8): 3291 - 3299. [Abstract] [Full Text] [PDF]

				H. Hernandez-Pigeon, C. Jean, A. Charruyer, M.-J. Haure, C. Baudouin, M. Charveron, A. Quillet-Mary, and G. Laurent UVA Induces Granzyme B in Human Keratinocytes through MIF: IMPLICATION IN EXTRACELLULAR MATRIX REMODELING J. Biol. Chem., March 16, 2007; 282(11): 8157 - 8164. [Abstract] [Full Text] [PDF]