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The cell surface receptor SLAM controls T cell and macrophage functions.
Ninghai Wang1, Abhay Satoskar, William Faubion
1Division of Immunology, RE-204, Beth Israel Deaconess Medical Center, Harvard Medical School, 41 Avenue Louis Pasteur, Boston, MA 02215, USA.
The Journal of Experimental Medicine
|May 5, 2004
Summary
Signaling lymphocyte activation molecule (SLAM) is crucial for immune responses. This study shows SLAM regulates T cell cytokine production and macrophage responses to LPS, impacting parasite clearance.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Signaling lymphocyte activation molecule (SLAM) is a glycoprotein on activated lymphocytes and antigen-presenting cells.
- SLAM regulates T cell responses and serves as a measles virus receptor.
Purpose of the Study:
- To investigate the role of SLAM in T cell activation and macrophage function.
- To determine SLAM's impact on innate and acquired immune responses.
Main Methods:
- Analysis of T cell receptor-induced cytokine secretion (IL-4, IFN-gamma) in SLAM(-/-) CD4(+) cells.
- Assessment of macrophage responses (IL-12, TNF, NO, phagocytosis) to LPS, peptidoglycan, and CpG in SLAM(-/-) cells.
- Evaluation of Leishmania major parasite clearance in SLAM(-/-) C57Bl/6 mice.
Main Results:
- T cell receptor-induced IL-4 secretion was down-regulated in SLAM(-/-) CD4(+) cells; IFN-gamma production was slightly up-regulated.
- SLAM controlled macrophage production of IL-12, TNF, and NO in response to LPS but not phagocytosis or responses to other TLR ligands.
- SLAM(-/-) mice exhibited defective macrophage function and an inability to clear Leishmania major parasites.
Conclusions:
- SLAM acts as a coreceptor regulating signals from Toll-like receptor 4 on macrophages.
- SLAM is essential for bridging innate and acquired immunity, particularly in host defense against parasitic infections.