LTB4 is an extremely pro-inflammatory lipid mediator that can exert its activity by binding to receptors BLT1
or BLT2 .
Serhan, "Resolvin E1 selectively interacts with leukotriene B4 receptor BLT1
and ChemR23 to regulate inflammation," Journal of Immunology, vol.
For instance, as is the case for c[PLA.sub.2][alpha]-deficient mice, mice lacking [LTC.sub.4] synthase ([LTC.sub.4]S), [LTD.sub.4] receptor (CysLT1), [LTB.sub.4] receptor (BLT1
), or [PGD.sub.2] receptor (DP1) are protected from asthma, (25-27) revealing the critical role of the c[PLA.sub.2][alpha]-[LTB.sub.4]/[LTC.sub.4]/[PGD.sub.2] axis in this allergic disease.
Leukotriene B4 signaling through NF-kappaB-dependent BLT1
receptors on vascular smooth muscle cells in atherosclerosis and intimal hyperplasia.
The LTs exert their actions through interaction with specific 7-transmembrane G-protein-coupled cell surface receptors, BLT1
and BLT2, representing the high and low-affinity receptor for LTB4, respectively, and CysLT1 receptor (CysLT1R) and CysLT2 receptor (CysLT2R) activated by the CysLTs [6, 7] plus a recently discovered LTE4-specific receptor known as CysLTER that was identified in [CysLT.sub.1]R/[CysLT.sub.2]R double-deficient mice .
Rola-Pleszczynski, "Involvement of BLT1
endocytosis and Yes kinase activation in leukotriene B4-induced neutrophil degranulation," The Journal of Immunology, vol.
have shown that mice lacking the gene encoding the LTB4 receptor, BLT1
, manifested decreased inflammation in adipose tissue and liver and were protected from systemic glucose and insulin intolerance compared to WT littermates .
Inhibition of atherogenesis in BLT1
-deficient mice reveals a role for LTB4 and BLT1
in smooth muscle cell recruitment.
Thus, the Elves of Tol Eressea in the Book of Lost Tales were small indeed, a notion that Tolkien would strongly regret later (BLT1
We also chose one gene (BLT1
) involved in the regulation of immune response and regulated by promoter hypermethylation (26).
Moreover, a recent study has demonstrated that LTB4 receptor 1 (BLT1
) and CXCR2 promoted the recruitment of neutrophils at psoriatic lesional sites and that these cells would secrete IL-1[beta], perpetuating psoriatic inflammation  (Table 1).
The involved cell surface receptors include macrophage mannose receptor, toll-like receptor 2 (TLR-2), C-type lectin receptor Dectin-1, and leukotriene B4 receptor (BLT1