Related Experiment Video

Updated: Jun 9, 2026

Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production
08:22

Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production

Published on: May 31, 2020

Bidirectional regulation by BACH2 coordinates systemic CXCR5- vs. CXCR5+ CD4+ T cell differentiation

Andrew R Schroeder1, Fangming Zhu1, Xianyou Xia1

  • 1Department of Microbiology, School of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.

The Journal of Experimental Medicine
|June 8, 2026
PubMed

CD4+ T cells differentiate into T follicular helper (Tfh) and non-Tfh cells, helping regulate humoral and cellular responses. Here, we show that in robust CD4+ T cell responses, all early CXCR5+CD4+ T cells expressed CD25, and STAT5, which inhibits Tfh cell differentiation, was crucial for both non-Tfh and Tfh responses. We found that after T cell activation, the transient increase in BACH2 protein levels temporarily suppressed STAT5-mediated Blimp1 induction, licensing early CXCR5+CD25+CD4+ T cells to proliferate to STAT5 signaling without being suppressed for the subsequent Tfh cell differentiation. Furthermore, depending on the immunization route, location, and antigen dose, BACH2 exerted bidirectional regulation on the differentiation of CXCR5- versus CXCR5+ CD4+ T cells throughout the body. Our findings suggest BACH2 orchestrates systemic immunity, offering insights for harnessing CD4+ T cell responses in vaccines and treatments.

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