受体
前列腺素D2
皮下注射
毒液
免疫学
化学
前列腺素E2
生物
趋化性
免疫球蛋白E
前列腺素
内分泌学
抗体
生物化学
作者
Misato Kida,Tatsuro Nakamura,Yuki Fujiwara,Masataka Nakamura,Takahisa Murata
标识
DOI:10.1096/fj.202002748rr
摘要
IgE-dependent/independent activation of mast cell (MC) has been assumed to play a host defensive role against venom injection in skin. However, its detailed mechanisms remain unknown. We aimed to investigate the contribution of MC-derived prostaglandin D2 (PGD2)-mediated signaling in host defense against bee venom (BV). To achieve this, we utilized gene-deficient mice of a PGD2 receptor, chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2). We first confirmed that subcutaneous injection of BV produced PGD2 equally in wild-type (WT) and CRTH2-deficient (Crth2−/−) mice skins. The BV injection dropped body temperature and impaired kidney equally in both lines of mice. In WT mice, pre-injection of BV (3 weeks) significantly inhibited the hypothermia and kidney impairment caused by second BV injection. In contrast, this pre-injection was not effective for the second BV injection in Crth2−/− mice. We also found that BV injections increased serum BV-specific IgE levels in WT mice, and its serum transfused mice improved the BV-induced hypothermia in naïve WT mice. In contrast, serum BV-specific IgE level was significantly lower in Crth2−/− mice. FACS analysis showed the BV injection stimulate migration of dendritic cells (DCs) into regional lymph nodes in WT mice. In Crth2−/− mice, its number was significantly smaller than that of WT mice. In conclusion, PGD2/CRTH2 signaling plays defensive role against second BV injection. This signaling promotes BV-specific IgE production at least partially by promoting DCs migration into regional lymph node.
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