| First Author | Wang N | Year | 2004 |
| Journal | J Exp Med | Volume | 199 |
| Issue | 9 | Pages | 1255-64 |
| PubMed ID | 15123745 | Mgi Jnum | J:90484 |
| Mgi Id | MGI:3043924 | Doi | 10.1084/jem.20031835 |
| Citation | Wang N, et al. (2004) The Cell Surface Receptor SLAM Controls T Cell and Macrophage Functions. J Exp Med 199(9):1255-64 |
| abstractText | 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 gamma 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. |
