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IgE-mediated regulation of IL-10 and type I IFN enhances rhinovirus-induced Th2 differentiation by primary human monocytes.
European Journal of Immunology ( IF 4.5 ) Pub Date : 2020-05-08 , DOI: 10.1002/eji.201948396 Regina K Rowe 1, 2, 3, 4 , David M Pyle 1, 3 , J David Farrar 1 , Michelle A Gill 1, 2, 3
European Journal of Immunology ( IF 4.5 ) Pub Date : 2020-05-08 , DOI: 10.1002/eji.201948396 Regina K Rowe 1, 2, 3, 4 , David M Pyle 1, 3 , J David Farrar 1 , Michelle A Gill 1, 2, 3
Affiliation
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Rhinovirus (RV) infections are linked to the development and exacerbation of allergic diseases including allergic asthma. IgE, another contributor to atopic disease pathogenesis, has been shown to regulate DC antiviral functions and influence T cell priming by monocytes. We previously demonstrated that IgE‐mediated stimulation of monocytes alters multiple cellular functions including cytokine secretion, phagocytosis, and influenza‐induced Th1 development. In this study, we investigate the effects of IgE‐mediated stimulation on monocyte‐driven, RV‐induced T cell development utilizing primary human monocyte‐T cell co‐cultures. We demonstrate that IgE crosslinking of RV‐exposed monocytes enhances monocyte‐driven Th2 differentiation. This increase in RV‐induced Th2 development was regulated by IgE‐mediated inhibition of virus‐induced type I IFN and induction of IL‐10. These findings suggest an additional mechanism by which two clinically significant risk factors for allergic disease exacerbations—IgE‐mediated stimulation and rhinovirus infection—may synergistically promote Th2 differentiation and allergic inflammation.
中文翻译：
IgE介导的对IL-10和I型IFN的调节可增强鼻病毒诱导的原代人单核细胞Th2分化。
鼻病毒（RV）感染与包括过敏性哮喘在内的过敏性疾病的发展和加剧有关。已证明，IgE是特应性疾病发病机理的另一个原因，它可调节DC抗病毒功能并影响单核细胞引发T细胞启动。我们先前证明了IgE介导的单核细胞刺激会改变多种细胞功能，包括细胞因子分泌，吞噬作用和流感病毒诱导的Th1发育。在这项研究中，我们调查了IgE介导的刺激对利用原代人单核细胞-T细胞共培养的单核细胞驱动，RV诱导的T细胞发育的影响。我们证明RV暴露的单核细胞的IgE交联会增强单核细胞驱动的Th2分化。RV诱导的Th2发育的这种增加受到IgE介导的病毒诱导的I型IFN抑制和IL-10诱导的调节。这些发现提示了一种额外的机制，通过该机制，两个临床上显着的变态反应性疾病恶化的危险因素（IgE介导的刺激和鼻病毒感染）可以协同促进Th2分化和变态反应性炎症。
更新日期：2020-05-08
中文翻译：
IgE介导的对IL-10和I型IFN的调节可增强鼻病毒诱导的原代人单核细胞Th2分化。
鼻病毒（RV）感染与包括过敏性哮喘在内的过敏性疾病的发展和加剧有关。已证明，IgE是特应性疾病发病机理的另一个原因，它可调节DC抗病毒功能并影响单核细胞引发T细胞启动。我们先前证明了IgE介导的单核细胞刺激会改变多种细胞功能，包括细胞因子分泌，吞噬作用和流感病毒诱导的Th1发育。在这项研究中，我们调查了IgE介导的刺激对利用原代人单核细胞-T细胞共培养的单核细胞驱动，RV诱导的T细胞发育的影响。我们证明RV暴露的单核细胞的IgE交联会增强单核细胞驱动的Th2分化。RV诱导的Th2发育的这种增加受到IgE介导的病毒诱导的I型IFN抑制和IL-10诱导的调节。这些发现提示了一种额外的机制，通过该机制，两个临床上显着的变态反应性疾病恶化的危险因素（IgE介导的刺激和鼻病毒感染）可以协同促进Th2分化和变态反应性炎症。
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