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The Journal of Immunology, 2008, 180: 7102-7106.
Copyright © 2008 by The American Association of Immunologists, Inc.
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Cutting Edge: Soluble IL-6R Is Produced by IL-6R Ectodomain Shedding in Activated CD4 T Cells1

Eva M. Briso, Oliver Dienz and Mercedes Rincon2

Department of Medicine/Immunobiology Program, University of Vermont, Burlington VT 05405

IL-6 trans-signaling via the soluble IL-6R (sIL-6R) plays an important role in the progression of several autoimmune diseases and cancer by providing IL-6-responsiveness to cells lacking IL-6R. However, the potential sources of sIL-6R are less understood. In this study we show that sIL-6R is produced by both naive and memory CD4 T cells upon TCR activation. The production of sIL-6R by activated CD4 T cells is mediated by shedding of the membrane-bound IL-6R, and this process correlates with the expression of the metalloproteinase ADAM17 in these cells. In contrast to CD4 T cells, CD8 T cells do not express ADAM17 and their production of sIL-6R is negligible. Thus, during an immune response CD4 T cells are an important source of sIL-6R. Production of sIL-6R by autoreactive CD4 T cells may contribute to their role in the development of autoimmune disease by conferring IL-6-responsiveness to cells lacking IL-6R such as synoviocytes.

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 National Institutes of Health Grant PO1 AI045666 (to M.R.).

2 Address correspondence and reprint requests to Dr. Mercedes Rincon, Department of Medicine/Immunobiology Division, Given Medical Building D305, University of Vermont, 89 Beaumont Avenue, Burlington, VT 05405. E-mail address: mrincon{at}uvm.edu

3 Abbreviations used in this paper: sIL-6R, soluble IL-6R; ADAM, a disintegrin and metalloproteinase domain; TAPI, TNF-{alpha} protease inhibitor.






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