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. 2019 Sep 4;10:2050. doi: 10.3389/fimmu.2019.02050

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Copyright © 2019 Zhang, Hu, Zhang, Yang, Peng, Zhang and Huang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Bach2 is down-regulated during Tfh cell differentiation and directly suppressed by BCL6. (A) Relative Bach2 mRNA abundance in naïve (CD44^lowCD62L^high), non-Tfh (CD44^highCD62L^lowCXCR5⁻PD1⁻), and Tfh cells isolated from the MLNs and/or spleens of WT mice at 2 months of age, determined by RT-qPCR. (B) The illustration depicting ChIP-seq tracks of BCL6 and indicated histone marks at the BACH2 gene in primary human Tfh cells. BCL6 binding peaks are shown at the top. (C) ChIP-qPCR analysis of BCL6 binding peak indicated by arrow in (B). The fold enrichment was calculated relative to IgG. Data are mean ± s.e.m. (D) The relative mRNA expression levels of Bach2 in Tfh cells sorted from the MLNs and spleens of 2-month-old WT and Bcl6^ERT2Cre mice 5 days post tamoxifen treatment. Data are mean ± s.e.m. of two mice per group. ^*P < 0.05 and ^**P < 0.01 (two-tailed t-test).