The mer receptor tyrosine kinase: Expression and function suggest a role in innate immunity

Edwards M. Behrens, Paul Gadue, Shun You Gong, Stacey Garrett, Paul L. Stein, Philip L. Cohen*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

92 Scopus citations


The mer receptor tyrosine kinase mediates phagocytosis of apoptotic cells and modulates cytokine production; it is also required for prevention of systemic autoimmune disease. Using a mer-specific antibody, we have confirmed the presence of mer on macrophages and now report its expression on NK cells, NKT cells, and dendritic cells (DC). We found that DC do not require mer for ingestion of apoptotic cells, as DC from mer-deficient mice phagocytose apoptotic cells normally. Mer was observed in splenic sections on cells outside follicular areas, probably representing DC and macrophages. Mer apparently participates in NKT-cell antigen-induced signaling, as NKT cells from mer-deficient mice evinced much lower cytokine production after in vivo α-galactosylceramide stimulation; this defect was intrinsic to the mer-deficient NKT cells. Taken together, these studies show mer expression on cells of the innate immune system. Mer, through its binding of lipid antigens, may not only mediate ingestion of apoptotic cells, but also signal events in NK cells, NKT cells, and DC.

Original languageEnglish (US)
Pages (from-to)2160-2167
Number of pages8
JournalEuropean Journal of Immunology
Issue number8
StatePublished - Aug 1 2003


  • Apoptosis
  • Autoimmunity
  • Innate immunity
  • Kinase
  • Phagocytosis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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