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首页> 外文期刊>Allergy >Siglec‐7 on peripheral blood eosinophils: Surface expression and function
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Siglec‐7 on peripheral blood eosinophils: Surface expression and function

机译：Siglec-7在外周血嗜酸性粒细胞：表面表达和功能

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Abstract Background Siglec‐7 is an inhibitory receptor ( IR ) expressed on human blood eosinophils. Whereas activation of other IR s, including Siglec‐8 and CD 300a, has been shown to downregulate eosinophil function, little is known about the role of Siglec‐7 on human eosinophils. Objective To examine Siglec‐7 expression and function in eosinophils from normal ( ND ) and eosinophilic ( EO ) donors. Methods Eosinophil expression of Siglec‐7 was quantified by flow cytometry and quantitative PCR . Soluble Siglec‐7 (sSiglec‐7) levels were measured by ELISA in serum. The effect of Siglec‐7 on eosinophil viability and degranulation was assessed in?vitro by AnnexinV‐ FITC /7‐ AAD staining and by measuring GM ‐ CSF ‐induced mediator release in culture supernatants. Signal transduction was studied by Western blot. Results Siglec‐7 was expressed ex?vivo on blood eosinophils from all eosinophilic and normal individuals studied. Siglec‐7 surface, but not SIGLEC ‐7 mRNA expression, was correlated with absolute eosinophil count ( AEC ). Siglec‐7 was upregulated on purified eosinophils after in?vitro stimulation with GM ‐ CSF or IL ‐5. Serum sSiglec‐7 was detectable in 133/144 subjects tested and correlated with AEC . Siglec‐7 cross‐linking inhibited GM ‐ CSF ‐induced release of eosinophil peroxidase, TNF ‐α, and IL ‐8 (n?=?7–8) but did not promote eosinophil apoptosis (n?=?5). Finally, Siglec‐7 cross‐linking on GM ‐ CSF ‐activated eosinophils induced phosphorylation of SHP ‐1 and de‐phosphorylation of ERK 1/2 and p38. Conclusions Siglec‐7 is constitutively expressed on human eosinophils and downmodulates eosinophil activation. Targeting of Siglec‐7 on eosinophils might enhance treatment efficacy in eosinophil‐driven disorders. Conversely, therapeutic interventions that inhibit Siglec‐7 could have unanticipated consequences and promote eosinophilic inflammation.
机译：摘要背景SigleC-7是在人血液粒细胞上表达的抑制受体（IR）。然而，除了在包括SigleC-8和Cd 300A的其他IR S的激活，已经显示为下调嗜酸性粒细胞函数，关于Siglec-7对人嗜酸性粒细胞的作用很少。目的检查来自正常（Nd）和嗜酸性粒细胞（EO）供体的嗜酸性粒细胞的Siglec-7表达和功能。方法通过流式细胞术和定量PCR量化SigleC-7的嗜酸性粒细胞表达。通过ELISA在血清中测量可溶性SIGLEC-7（SSIGLEC-7）水平。通过annexinv-fitc / 7- aad染色来评估Siglec-7对嗜酸性粒细胞活力和脱粒的影响，并通过测定培养上清液中的介质介质释放。通过Western印迹研究了信号转导。结果Siglec-7表达了来自所有嗜酸性嗜嗜酸性和正常个体的血嗜酸性粒细胞的体内。 Siglec-7表面，但不是SigleC -7 mRNA表达，与绝对嗜酸性粒细胞计数（AEC）相关。在用GM - CSF或IL -5的体外刺激后纯化的嗜酸性粒细胞上调Siglec-7。在测试和与AEC进行的133/144受试者中可检测到血清SSIGLEC-7。 Siglec-7交联抑制的GM - CSF诱导嗜酸性粒细胞过氧化物酶的释放，TNF-α和IL -8（n？= 7-8），但未促进嗜酸性粒细胞凋亡（n？=？5）。最后，SigleC-7对GM - CSF-activated嗜酸性粒细胞的交联诱导SHP -1的磷酸化和ERK 1/2和P38的去磷酸化。结论Siglec-7在人嗜酸性粒细胞上构成思考和司嗜酸氢粒细胞激活。 Siglec-7对嗜酸性粒细胞的靶向可能会增强嗜酸性粒细胞驱动障碍的治疗效果。相反，抑制Siglec-7的治疗干预措施可能具有意外的后果和促进嗜酸性炎症。

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