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Differential regulation by leukotrienes and calcium of Fcγ receptor‐induced phagocytosis and Syk activation in dendritic cells versus macrophages
Author(s) -
Canetti Claudio,
Aronoff David M.,
Choe Mun,
Flamand Nicolas,
Wettlaufer Scott,
Toews Galen B.,
Chen GwoHsiao,
PetersGolden Marc
Publication year - 2006
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0705374
Subject(s) - syk , biology , phagocytosis , microbiology and biotechnology , leukotriene b4 , fc receptor , efferocytosis , immunology , proinflammatory cytokine , immune system , signal transduction , tyrosine kinase , inflammation , macrophage , in vitro , biochemistry
Macrophage (MØ) phagocytosis via the Fc receptor for immunoglobulin G (FcγR) requires the spleen tyrosine kinase (Syk) and serves an important antimicrobial function. We have reported previously that FcγR‐mediated ingestion and Syk activation in MØ are amplified by and depend on the proinflammatory lipid mediator leukotriene B 4 (LTB 4 ). Although FcγR‐mediated ingestion is also important for antigen uptake, there is no information about LTB 4 regulation of these processes in dendritic cells (DCs). In this study, we compared murine bone marrow (BM)‐derived DCs to MØ from BM, peritoneum, and the pulmonary alveolar space. Neither phagocytosis nor Syk activation in DCs was influenced by exogenous LTB 4 . Unlike the various MØ populations, Syk activation in DCs was likewise unaffected by pharmacologic or genetic strategies to inhibit endogenous LTB 4 synthesis or to block the high‐affinity LTB 4 receptor BLT1. DCs were refractory to regulation by LTB 4 despite the fact that they expressed BLT1 and mobilized intracellular calcium in response to its ligation. This resistance to LTB 4 in DCs instead reflected the fact that in contrast to MØ, Syk activation in DCs was itself entirely independent of calcium. These results identify a fundamental difference in FcγR signaling between DCs and MØ, which may relate to the divergent, functional consequences of target ingestion in the two cell types.