TREM-2 (triggering receptor expressed on myeloid cells 2) is a phagocytic receptor for bacteria.

Phagocytosis, which is essential for the immune response to pathogens, is
initiated by specific interactions between pathogens and cell surface receptors
expressed by phagocytes. This study identifies triggering receptor expressed on
myeloid cells 2 (TREM-2) and its signaling counterpart DAP12 as a molecular
complex that promotes phagocytosis of bacteria. Expression of TREM-2-DAP12
enables nonphagocytic Chinese hamster ovary cells to internalize bacteria. This
function depends on actin cytoskeleton dynamics and the activity of the small
guanosine triphosphatases Rac and Cdc42. Internalization also requires src kinase
activity and tyrosine phosphorylation. In bone marrow-derived macrophages,
phagocytosis is decreased in the absence of DAP12 and can be restored by
expression of TREM-2-DAP12. Depletion of TREM-2 inhibits both binding and uptake
of bacteria. Finally, TREM-2-dependent phagocytosis is impaired in Syk-deficient
macrophages. This study highlights a novel role for TREM-2-DAP12 in the immune
response to bacterial pathogens.
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