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趋化因子冗余与特异性:以 CXCR3 及其配体为例。

Chemokine redundancy versus specificity in the context of CXCR3 and its ligands.

机构信息

Wellcome Centre for Cell-Matrix Research, Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.

Northern Care Alliance NHS Group, Geoffrey Jefferson Brain Research Centre, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.

出版信息

Immunol Cell Biol. 2022 Jul;100(6):387-389. doi: 10.1111/imcb.12553. Epub 2022 May 10.

DOI:10.1111/imcb.12553
PMID:35466477
Abstract

In a recent article published in Immunology & Cell Biology, Dalit et al. describe how correcting mutations in the C57BL/6 mouse strain can restore production of the chemokine CXCL11, although surprisingly, this expression of CXCL11 had little effect on B and T cells and the innate immune response to infection with lymphocytic choriomeningitis virus or influenza virus.

摘要

在最近发表在《免疫学与细胞生物学》上的一篇文章中,Dalit 等人描述了如何纠正 C57BL/6 小鼠品系中的突变,以恢复趋化因子 CXCL11 的产生,但令人惊讶的是,这种 CXCL11 的表达对 B 和 T 细胞以及对淋巴细胞性脉络丛脑膜炎病毒或流感病毒感染的先天免疫反应几乎没有影响。

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