The Cell Surface Receptor SLAM Controls T Cell and Macrophage Functions

Ninghai Wang, Abhay Satoskar, William Faubion, Duncan Howie, Susumu Okamoto, Stefan Feske, Charles Gullo, Kareem Clarke, Miriam Rodriguez Sosa, Arlene H. Sharpe, Cox Terhorst

Research output: Contribution to journalArticlepeer-review

140 Scopus citations


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-/- C57B1/6 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.

Original languageEnglish (US)
Pages (from-to)1255-1264
Number of pages10
JournalJournal of Experimental Medicine
Issue number9
StatePublished - May 3 2004


  • L. major
  • Macrophage
  • SLAM
  • T cell

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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