贝赫切特病患者中异常的单核细胞亚群。
Aberrant monocyte subsets in patients with Behçet's disease.
机构信息
Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, The Ministry of Education Key Laboratory, National Clinical Research Center for Dermatologic and Immunologic Diseases, State Key Laboratory of Complex Severe and Rare Diseases, Shuaifuyuan, Dongcheng District, Beijing 100730, China; Department of Rheumatology,Peking University Shougang Hospital, Beijing 100144, China.
Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, The Ministry of Education Key Laboratory, National Clinical Research Center for Dermatologic and Immunologic Diseases, State Key Laboratory of Complex Severe and Rare Diseases, Shuaifuyuan, Dongcheng District, Beijing 100730, China.
出版信息
Clin Immunol. 2021 Apr;225:108683. doi: 10.1016/j.clim.2021.108683. Epub 2021 Feb 5.
Monocytes are a versatile and dynamic population, but its implication in Behçet's Disease (BD) remains elusive. We investigated the proportion, phenotypical and functional alterations in classical monocytes (CM), intermediate monocytes (IM) and non-classical monocytes (NCM) subsets in BD. A higher IM and lower NCM population in BD patients were noted, closely correlated with disease activity, and rescued after treatment. CD11b and CD64 expression on CM, IM and NCM in BD were enhanced. BD CM promoted TNF-a and IL-6 production and facilitated Th1 differentiation. BD IM promoted IL-6 production. We further demonstrated a higher level of phosphorylated p65 (p-p65) in BD CM and increased p-p65 and p-p38 in BD IM. Our data highlighted the aberrant populations of IM and CM in BD, potentially implicated in BD' pathogenesis.
单核细胞是一种多功能且具有动态变化的细胞群体，但它在白塞病（BD）中的作用仍不清楚。我们研究了 BD 患者经典单核细胞（CM）、中间单核细胞（IM）和非经典单核细胞（NCM）亚群中的比例、表型和功能变化。我们发现 BD 患者的 IM 比例较高，NCM 比例较低，且与疾病活动度密切相关，经治疗后得到恢复。BD 患者 CM、IM 和 NCM 上的 CD11b 和 CD64 表达增强。BD CM 促进 TNF-a 和 IL-6 的产生，并有利于 Th1 分化。BD IM 促进 IL-6 的产生。我们进一步证明了 BD CM 中磷酸化 p65（p-p65）水平较高，BD IM 中 p-p65 和 p-p38 增加。我们的数据强调了 BD 中 IM 和 CM 的异常群体，它们可能与 BD 的发病机制有关。
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