Phenotypic Tfh development promoted by CXCR5-controlled re-localization and IL-6 from radiation-resistant cells.
10.1007/s13238-015-0210-0
- Author:
Xin CHEN
1
;
Weiwei MA
2
;
Tingxin ZHANG
2
;
Longyan WU
2
;
Hai QI
3
Author Information
1. Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing, 100084, China. xin.chen01@foxmail.com.
2. Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing, 100084, China.
3. Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing, 100084, China. qihai@tsinghua.edu.cn.
- Publication Type:Journal Article
- Keywords:
Bcl6;
CXCR5;
IL-6;
Tfh;
radiation-resistant cell
- MeSH:
Animals;
CD40 Ligand;
metabolism;
Cell Differentiation;
physiology;
DNA-Binding Proteins;
metabolism;
Inducible T-Cell Co-Stimulator Protein;
metabolism;
Interleukin-6;
metabolism;
Mice;
Proto-Oncogene Proteins c-bcl-6;
Receptors, CXCR5;
metabolism;
T-Lymphocytes, Helper-Inducer;
metabolism
- From:
Protein & Cell
2015;6(11):825-832
- CountryChina
- Language:English
-
Abstract:
How follicular T-helper (Tfh) cells develop is incompletely understood. We find that, upon antigen exposure in vivo, both naïve and antigen-experienced T cells sequentially upregulate CXCR5 and Bcl6 within the first 24 h, relocate to the T-B border, and give rise to phenotypic Bcl6(+)CXCR5(+) Tfh cells before the first cell division. CXCR5 upregulation is more dependent on ICOS costimulation than that of Bcl6, and early Bcl6 induction requires T-cell expression of CXCR5 and, presumably, relocation toward the follicle. This early and rapid upregulation of CXCR5 and Bcl6 depends on IL-6 produced by radiation-resistant cells. These results suggest that a Bcl6(hi)CXCR5(hi) phenotype does not automatically define a Tfh lineage but might reflect a state of antigen exposure and non-commitment to terminal effector fates and that niches in the T-B border and/or the follicle are important for optimal Bcl6 induction and maintenance.
