表达IL-17F的人CD4 + T细胞的存在，功能和调控。,European Journal of Immunology

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表达IL-17F的人CD4 + T细胞的存在，功能和调控。
European Journal of Immunology ( IF 4.5 ) Pub Date : 2020-01-16 , DOI: 10.1002/eji.201948138
Lachrissa A Burns ₁ , Ash Maroof ₂ , Diane Marshall ₂ , Kathryn J A Steel ₁ , Sylvine Lalnunhlimi ₁ , Suzanne Cole ₂ , Anca Catrina ₃ , Bruce Kirkham ₄ , Leonie S Taams ₁

Affiliation

促炎细胞因子IL-17A已经牵涉到炎性关节炎的免疫病理学中。IL-17F与IL-17A具有50％的同源性，最近被认为在炎症中起作用。我们调查了IL-17F + CD4 + T细胞的诱导和细胞因子分布，以及IL-17F如何可能导致炎症。在用IL-1β，IL-23，抗CD3和抗CD28 mAb培养健康的供体CD4 + T细胞后，检测到了表达IL-17A和IL-17F的细胞。与IL-17A + IL-17F- CD4 + T细胞相比，IL-17F + IL-17A-和IL-17A + IL-17F + CD4 + T细胞所含IL-10表达细胞和GM-CSF表达细胞的比例较低，且比例较高表达IFN-γ的细胞。抗CD28 mAb的滴定显示，强共刺激可增加IL-17F + IL-17A-和IL-17A + IL-17F + CD4 + T细胞的频率，而IL-17A + IL-17F- CD4 + T细胞频率降低。这部分是通过IL-2依赖性机制介导的。向炎性关节炎患者的滑膜成纤维细胞中添加IL-17A，IL-17F和TNF-α会导致IL-6和IL-8的大量产生，通过联合阻断IL-17A和IL-17F比单独的IL-17A封锁要好。我们的数据表明，IL-17A和IL-17F在T细胞共同刺激时受到差异调节，并且与单独的IL-17A阻断相比，IL-17A和IL-17F的双重阻断更有效地减轻了炎症。与单独的IL-17A阻断相比，IL-17A和IL-17F的联合阻断作用在更大程度上降低了抗凝作用。我们的数据表明，IL-17A和IL-17F在T细胞共同刺激时受到差异调节，并且与单独的IL-17A阻断相比，IL-17A和IL-17F的双重阻断更有效地减轻了炎症。与单独的IL-17A阻断相比，IL-17A和IL-17F的联合阻断作用在更大程度上降低了抗凝作用。我们的数据表明，IL-17A和IL-17F在T细胞共同刺激时受到差异调节，并且与单独的IL-17A阻断相比，IL-17A和IL-17F的双重阻断更有效地减轻了炎症。

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Presence, function, and regulation of IL-17F-expressing human CD4+ T cells.

The pro-inflammatory cytokine IL-17A has been implicated in the immunopathology of inflammatory arthritis. IL-17F bears 50% homology to IL-17A and has recently been suggested to play a role in inflammation. We investigated the induction and cytokine profile of IL-17F+ CD4+ T cells, and how IL-17F may contribute to inflammation. Upon culture of healthy donor CD4+ T cells with IL-1β, IL-23, anti-CD3, and anti-CD28 mAb, both IL-17A and IL-17F-expressing cells were detected. In comparison to IL-17A+ IL-17F- CD4+ T cells, IL-17F+ IL-17A- and IL-17A+ IL-17F+ CD4+ T cells contained lower proportions of IL-10-expressing and GM-CSF-expressing cells and higher proportions of IFN-γ-expressing cells. Titration of anti-CD28 mAb revealed that strong co-stimulation increased IL-17F+ IL-17A- and IL-17A+ IL-17F+ CD4+ T cell frequencies, whereas IL-17A+ IL-17F- CD4+ T cell frequencies decreased. This was partly mediated via an IL-2-dependent mechanism. Addition of IL-17A, IL-17F, and TNF-α to synovial fibroblasts from patients with inflammatory arthritis resulted in significant production of IL-6 and IL-8, which was reduced to a larger extent by combined blockade of IL-17A and IL-17F than blockade of IL-17A alone. Our data indicate that IL-17A and IL-17F are differentially regulated upon T cell co-stimulation, and that dual blockade of IL-17A and IL-17F reduces inflammation more effectively than IL-17A blockade alone.

更新日期：2020-01-16

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