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TLT2 Functions as an Inhibitory Receptor that Attenuates the Oxidative Burst In Neutrophils Stimulated with FMLP
Author(s) -
Halpert Matthew M,
King R. Glenn,
Justement Louis
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.672.56
Subject(s) - microbiology and biotechnology , receptor , respiratory burst , innate immune system , biology , formyl peptide receptor , chemotaxis , inflammation , chemokine , downregulation and upregulation , haematopoiesis , signal transduction , immunology , biochemistry , gene , stem cell
Trem Like Transcript 2 (TLT2) is a recently identified member of the Triggering Receptor Expressed on Monocyte (TREM) locus. Analysis of TLT2 expression by cells of the hematopoietic lineage revealed that this receptor is expressed on B lineage cells, making it the only conserved member of the TREM locus to be expressed on lymphocytes. Within the mature B cell compartment, TLT2 expression is highest on the B1 and marginal zone populations, although it is expressed on virtually all follicular B cells as well. Aside from B cells, TLT2 is expressed on macrophages as well as neutrophils in the bone marrow and periphery. Treatment of mice with agents that induce inflammation results in a dramatic increase in the level of TLT2 expressed on activated neutrophils. Because TLT2 is expressed at higher levels on innate‐like B cells, macrophages and neutrophils, and is upregulated in response to inflammatory stimuli, it is likely that this receptor plays a role in innate immunity. Recent studies have demonstrated that ligation of TLT2 inhibits the oxidative burst in neutrophils stimulated with FMLP. These results suggest that TLT2 may function as an inhibitory receptor that attenuates activation of neutrophils, and possibly macrophages, stimulated with agonists that bind to seven transmembrane‐spanning receptors that signal via heterotrimeric G‐proteins.