Mast cells, neuropeptides, histamine, and prostaglandins in UV-induced systemic immunosuppression

Mast cells, neuropeptides, histamine, and prostaglandins in UV-induced systemic immunosuppression
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DOI:
10.1016/s1046-2023(02)00201-3
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发表时间:
2002-09-01
期刊:
影响因子:
4.8
通讯作者:
Finlay-Jones, JJ
Finlay-Jones, JJ
中科院分区:
生物学3区
文献类型:
--
作者:
Hart, PH;Townley, SL;Finlay-Jones, JJ

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不同品系小鼠背部皮肤中真皮肥大细胞的发生率与对UVB诱导的全身免疫抑制的易感性有直接关系;对紫外线高度敏感的C57BL/6小鼠的真皮肥大细胞发生率较高,而BALB/c小鼠的真皮肥大细胞发生率较低,而BALB/c小鼠需要相当大的紫外线辐射才能达到50%的免疫抑制。真皮肥大细胞的流行与UVB和顺式尿毒酸(UCA)诱导的全身免疫抑制的易感性之间也存在功能上的联系。肥大细胞耗竭的小鼠对UVB或顺式UCA的全身免疫抑制没有反应,除非它们事先在照射或顺式UCA给药的部位与骨髓来源的肥大细胞前体重建。顺式UCA不直接刺激肥大细胞脱颗粒。相反,为了支持研究表明UVB和cis-UCA在辣椒素治疗的神经肽缺乏的小鼠中都没有免疫抑制作用,cis-UCA刺激的神经肽从感觉c纤维释放,进而可以有效地使肥大细胞脱颗粒。对小鼠的研究表明,组胺而不是肿瘤坏死因子α(TNF-α)是肥大细胞刺激下游免疫抑制的产物。组胺受体拮抗剂减少了大约60%的UVB和顺式UCA诱导的全身免疫抑制。消炎痛对小鼠的作用与组胺受体拮抗剂无累加效应。组胺可以刺激角质形成细胞产生前列腺素。我们认为组胺和前列腺素E-2在下游免疫抑制中都是重要的;两者都是支持T辅助2细胞发育和减少I型免疫反应(如接触性超敏反应)表达的调节分子。(C)2002年埃尔塞维尔科学公司(美国)。版权所有。
There is a direct correlation between dermal mast cell prevalence in dorsal skin of different mouse strains and susceptibility to UVB-induced systemic immunosuppression; highly UV-susceptible C57BL/6 mice have a high dermal mast cell prevalence while BALB/c mice, which require considerable UV radiation for 50% immunosuppression, have a low mast cell prevalence. There is also a functional link between the prevalence of dermal mast cells and susceptibility to UVB- and cis-urocanic acid (UCA)-induced systemic immunosuppression. Mast cell-depleted mice are unresponsive to UVB or cis-UCA for systemic immunosuppression unless they are previously reconstituted at the irradiated or cis-UCA-administered site with bone marrow-derived mast cell precursors. cis-UCA does not stimulate mast cell degranulation directly. Instead, in support of studies showing that neither UVB nor cis-UCA was immunosuppressive in capsaicin-treated, neuropeptide-depleted mice, cis-UCA-stimulated neuropeptide release from sensory c-fibers which, in turn, could efficiently degranulate mast cells. Studies in mice suggested that histamine, and not tumor necrosis factor alpha (TNF-alpha), was the product from mast cells that stimulated downstream immuno suppression. Histamine receptor antagonists reduced by approximately 60% UVB and cis-UCA-induced systemic immunosuppression. Indomethacin administration to mice had a similar effect which was not cumulative with the histamine receptor antagonists. Histamine can stimulate keratinocyte prostanoid production. We propose that both histamine and prostaglandin E-2 are important in downstream immunosuppression; both are regulatory molecules supporting the development of T helper 2 cells and reduced expression of type I immune responses such as a contact hypersensitivity reaction. (C) 2002 Elsevier Science (USA). All rights reserved.