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-/- 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 language | English (US) |
---|---|
Pages (from-to) | 1255-1264 |
Number of pages | 10 |
Journal | Journal of Experimental Medicine |
Volume | 199 |
Issue number | 9 |
DOIs | |
State | Published - May 3 2004 |
Keywords
- L. major
- Macrophage
- SLAM
- T cell
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology