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Updated: Oct 22, 2025

Evaluation of T Follicular Helper Cells and Germinal Center Response During Influenza A Virus Infection in Mice
Published on: June 27, 2020
BCL6 controls contact-dependent help delivery during follicular T-B cell interactions
Dan Liu1, Jiacong Yan2, Jiahui Sun1
1Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing 100084, China; Laboratory of Dynamic Immunobiology, Institute for Immunology, Tsinghua University, Beijing 100084, China; Department of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing 100084, China.
BCL6 is crucial for follicular helper T (Tfh) cell development and germinal center (GC) formation. This study reveals BCL6 regulates Tfh cell signaling and B cell interactions, essential for GC maintenance.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Follicular helper T (Tfh) cells are essential for germinal center (GC) formation and antibody responses.
- BCL6 is a known master regulator of Tfh cell differentiation, but its precise functions in GC formation remain incompletely understood.
Purpose of the Study:
- To elucidate the unique functions of BCL6 in T cells that are essential for germinal center formation.
- To investigate how BCL6 deficiency impacts Tfh cell function and interactions with B cells.
Main Methods:
- Conditional knockout mouse models to ablate BCL6 alleles in T cells.
- Flow cytometry to analyze Tfh cell populations and activation markers.
- In vivo imaging to assess T cell-B cell interactions and CD40L delivery.
Main Results:
- BCL6 haploinsufficiency impaired GC formation and Tfh cell maintenance without affecting early T cell activation or localization.
- BCL6 was found to regulate Tfh cell calcium signaling and CD40L delivery to B cells.
- Overexpression of CD40L rescued GC formation and Tfh cell maintenance defects in BCL6-haploinsufficient mice.
Conclusions:
- BCL6 plays critical roles in Tfh cell signaling and B cell interactions, which are essential for GC formation.
- BCL6 maintains Tfh cell phenotypes in a non-autonomous manner, highlighting its importance beyond T cell intrinsic functions.
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