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宿主miR-135a对免疫反应的调节作用。 （注：原英文文本“Modulation of Immune Response to by Host miR-135a.”中“to”后面似乎缺少内容）

Modulation of Immune Response to by Host miR-135a.

作者信息

Keck Jonathon, Chambers James P, Yu Jieh-Juen, Cheng Xingguo, Christenson Lane K, Guentzel M N, Gupta Rishein, Arulanandam Bernard P

机构信息

South Texas Center for Emerging Infectious Diseases, Department of Biology, University of Texas at San Antonio, San Antonio, TX, United States.

Department of Materials & Bioengineering, Southwest Research Institute, San Antonio, TX, United States.

出版信息

Front Cell Infect Microbiol. 2021 Apr 13;11:638058. doi: 10.3389/fcimb.2021.638058. eCollection 2021.

DOI:10.3389/fcimb.2021.638058
PMID:33928045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8076868/
Abstract

Previously, our laboratory established the role of small, noncoding RNA species, microRNA (miRNA) including miR-135a in anti-chlamydial immunity in infected hosts. We report here chlamydial infection results in decreased miR-135a expression in mouse genital tissue and a fibroblast cell line. Several chemokine and chemokine receptor genes (including CXCL10, CCR5) associated with chlamydial pathogenesis were identified to contain putative miR-135a binding sequence(s) in the 3' untranslated region. The role of miR-135a in the host immune response was investigated using exogenous miR-135a mimic to restore the immune phenotype associated with decreased miR-135a following (Cm) infection. We observed miR-135a regulation of Cm-primed bone marrow derived dendritic cells (BMDC) activation of Cm-immune CD4 T cells for clonal expansion and CCR5 expression. Using a transwell cell migration assay, we explore the role of miR-135a in regulation of genital tract CXCL10 expression and recruitment of CXCR3 CD4 T cells the CXCL10/CXCR3 axis. Collectively, data reported here support miR-135a affecting multiple cellular processes in response to chlamydial infection.

摘要

此前，我们实验室确定了包括miR - 135a在内的小的非编码RNA物种——微小RNA（miRNA）在受感染宿主抗衣原体免疫中的作用。我们在此报告，衣原体感染导致小鼠生殖组织和成纤维细胞系中miR - 135a表达降低。已确定几个与衣原体发病机制相关的趋化因子和趋化因子受体基因（包括CXCL10、CCR5）在3'非翻译区含有假定的miR - 135a结合序列。使用外源性miR - 135a模拟物来恢复感染（Cm）后与miR - 135a降低相关的免疫表型，研究了miR - 135a在宿主免疫反应中的作用。我们观察到miR - 135a对经Cm致敏的骨髓来源树突状细胞（BMDC）激活经Cm免疫的CD4 T细胞进行克隆扩增和CCR5表达的调节作用。使用Transwell细胞迁移试验，我们探讨了miR - 135a在调节生殖道CXCL10表达以及通过CXCL10/CXCR3轴招募CXCR3 CD4 T细胞中的作用。总体而言，此处报告的数据支持miR - 135a在响应衣原体感染时影响多个细胞过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/8076868/f53cdb135d7c/fcimb-11-638058-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/8076868/07d85650aff4/fcimb-11-638058-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/8076868/542d49f8ad90/fcimb-11-638058-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/8076868/f53cdb135d7c/fcimb-11-638058-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/8076868/07d85650aff4/fcimb-11-638058-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/8076868/542d49f8ad90/fcimb-11-638058-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5b0/8076868/f53cdb135d7c/fcimb-11-638058-g003.jpg

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