Document Type
Article
Publication Date
Spring 5-3-2004
Abstract
Signaling lymphocyte activation molecule (SLAM), a glycoprotein expressed on activated lymphocytes and antigen-presenting cells, has been shown to be a coregulator of antigen-driven T cell responses and is one of the two receptors for measles virus. Here we show that T cell receptor–induced interleukin (IL)-4 secretion by SLAM−/− CD4+ cells is down-regulated, whereas interferon γ production by CD4+ T cells is only slightly up-regulated. Although SLAM controls production of IL-12, tumor necrosis factor, and nitric oxide in response to lipopolysaccharide (LPS) by macrophages, SLAM does not regulate phagocytosis and responses to peptidoglycan or CpG. Thus, SLAM acts as a coreceptor that regulates signals transduced by the major LPS receptor Toll-like receptor 4 on the surface of mouse macrophages. A defective macrophage function resulted in an inability of SLAM−/− C57Bl/6 mice to remove the parasite Leishmania major. We conclude that the coreceptor SLAM plays a central role at the interface of acquired and innate immune responses.
Recommended Citation
Wang N, Satoskar A, Faubion W, Howie D, Okamoto S, et al. 2004. The cell surface receptor SLAM controls T cell and macrophage functions. J. Exp. Med. 199:1255–64
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Medical Biochemistry Commons, Medical Cell Biology Commons, Medical Specialties Commons, Other Medical Sciences Commons
Comments
The copy of record and supplemental material are available from the publisher at http://www.jem.org/cgi/doi/10.1084/jem.20031835. Copyright 2004 The Rockefeller University Press and The Authors. All rights reserved.