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The Chemokine CCL6 Promotes Innate Immunity via Immune Cell Activation and Recruitment¹

Ana L. Coelho^2,*, Matthew A. Schaller^*, Claudia F. Benjamim, Amos Z. Orlofsky, Cory M. Hogaboam^* and Steven L. Kunkel^*

^* Department of Pathology, University of Michigan, Ann Arbor, Michigan 48109; Department of Pharmacology, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil; Albert Einstein College of Medicine, Yeshiva University, Bronx, NY 10461

Septic syndrome is a consequence of innate immune failure. Recent studies showed that the CC chemokine CCL6 enhanced antimicrobial immunity during experimental sepsis through an unknown mechanism. The present study demonstrates that transgenic CCL6 expression abolishes mortality in a septic peritonitis model via the modulation of resident peritoneal cell activation and, more importantly, through the recruitment of IFN-producing NK cells and killer dendritic cells into the peritoneum. Thus, CCL6 attenuates the immune failure during sepsis, in part, through a protective type 1-cytokine mediated mechanism.

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 National Institutes of Health (P50 HL 056402, P01 HL 031963, and R01 HL031237).

² Address correspondence and reprint requests to Dr. Ana L. Coelho, Department of Pathology, University of Michigan, 109 Zina Pitcher Place, Ann Arbor, Michigan 48109. E-mail address: analuci{at}med.umich.edu

³ Abbreviations used in this paper: SIRS, systemic inflammatory response syndrome; CARS, compensatory anti-inflammatory response; CLP, cecal ligation and puncture; CCL6 Tg, transgenically overexpressing CCL6; IKDC, IFN-producing killer dendritic cell; WT, wild type; AST, aspartate transaminase; ALT, alanine transaminase; PC, peritoneal cavity; DC, dendritic cell; MHCII, MHC class II.

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