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首页> 外文期刊>Allergy >In human basophils, IL-3 selectively induces RANKL expression that is modulated by IgER-dependent and IgER-independent stimuli
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In human basophils, IL-3 selectively induces RANKL expression that is modulated by IgER-dependent and IgER-independent stimuli

机译：在人嗜碱性粒细胞中，IL-3选择性地诱导由inger依赖和艾格尔无关的刺激调节的RANKL表达

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Results We show that in human basophils, IL-3 but no other stimulus induces de novo expression of soluble and surface RANKL, of which the latter enhances survival of MoDC. Upon simultaneous stimulation, IgER cross-linking reduces surface RANKL expression, while IgER-independent stimuli have no effect. This is in contrast to consecutive stimulation, as triggering with both IgER-dependent and IgER-independent stimuli enhances RANKL expression, particularly in its soluble form. Real-time PCR analysis shows that RANKL expression is mainly regulated at the mRNA level.Conclusion This study identifies IL-3 as a potent inducer of RANKL expression in human basophils, suggesting them to interact with bone physiology and activation of immune cells. IgER-dependent and IgER-independent stimuli modulate the IL-3-mediated RANKL expression in a time- and stimulus-dependent fashion.Methods Among other stimuli, basophils were cultured with IL-3 alone. Alternatively, as a secondary stimulus, IgER-dependent or IgER-independent agents were added simultaneously either with IL-3 or after prolonged IL-3 culturing. Expression of RANKL protein and mRNA was analyzed by flow cytometry, ELISA, and real-time PCR. A coculture system was applied to investigate biological activity of basophil-derived RANKL.Background Receptor activator of NF-κB ligand (RANKL) is expressed as either surface (hRANKL1, hRANKL2) or soluble (hRANKL3) form. RANKL is involved in multifaceted processes of immunoregulation and bone resorption such as they occur in rheumatoid arthritis (RA). Interestingly, activated basophils, which are effector cells in allergic inflammation, contribute to the progress of collagen-induced arthritis (CIA), a mouse model for RA. Here, we investigate under which conditions human basophils express RANKL.
机译：结果表明，在人类嗜碱性粒细胞中，IL-3但没有其他刺激诱导易溶性和表面RANKL的表达，其中后者增强了MODC的存活率。同时刺激后，IGEL交联减少了表面RANKL表达，而Iger-Indooll-Iss-Cnotting Readling表达无效。这与连续的刺激相反，与依赖于IGER依赖性和无关的刺激的触发增强了RANKL表达，特别是其可溶性形式。实时PCR分析表明，RANKL表达主要受到MRNA水平的调节。结论本研究将IL-3鉴定为人类嗜碱性粒细胞中RANKL表达的有效诱导剂，表明它们与骨生理学和免疫细胞的激活相互作用。 inger依赖性和艾格尔无关的刺激在时间和刺激依赖的时尚中调节IL-3介导的RANKL表达。其他刺激等中的方法，单独用IL-3培养嗜碱性粒细胞。或者，作为二级刺激，同时用IL-3或延长IL-3培养后同时加入Iger依赖性或无关的试剂。通过流式细胞术，ELISA和实时PCR分析RANKL蛋白和mRNA的表达。应用了共培养系统来研究嗜碱性粒细胞衍生的RANKL.BACHGRONGRGGETCOR（RANKL）的Background受体活化剂的生物活性，表示为表面（HRANKL1，HRANKL2）或可溶性（HRANKL3）形式。 Rankl参与了多方面的免疫调节和骨吸收过程，例如它们在类风湿性关节炎（RA）中发生。有趣的是，作为过敏性炎症中的效应细胞的活化嗜碱性嗜碱基，有助于胶原蛋白诱导的关节炎（CIA）的进展，RA的小鼠模型。在这里，我们调查人类嗜碱性粒细胞表达RANKL的条件下。

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