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A role for Hes1 in constraining germinal center B cell formation()

Germinal center is a transient lymphoid tissue structure in which B cells undergo affinity maturation and differentiate into memory B cells and plasma cells. GC formation depends on B cell expression of BCL6, a master transcription regulator of the GC state. Bcl6 expression is under elaborate contro...

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Detalles Bibliográficos
Autores principales: Shao, Xingxing, Liu, Xin, Qi, Hai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10134198/
https://www.ncbi.nlm.nih.gov/pubmed/37193067
http://dx.doi.org/10.1016/j.cellin.2023.100078
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author Shao, Xingxing
Liu, Xin
Qi, Hai
author_facet Shao, Xingxing
Liu, Xin
Qi, Hai
author_sort Shao, Xingxing
collection PubMed
description Germinal center is a transient lymphoid tissue structure in which B cells undergo affinity maturation and differentiate into memory B cells and plasma cells. GC formation depends on B cell expression of BCL6, a master transcription regulator of the GC state. Bcl6 expression is under elaborate control by external signals. HES1 plays important roles in T-cell lineage commitment, although little is known about its potential roles in GC formation. Here we report that B-cell-specific HES1 deletion causes a significant increase in GC formation, leading to increased production of plasma cells. We further provide evidence that HES1 inhibits BCL6 expression in a bHLH domain-dependent manner. Our study suggests a new layer of regulation of GC initiation mediated by HES1 and, by inference, Notch signals in vivo.
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spelling pubmed-101341982023-05-15 A role for Hes1 in constraining germinal center B cell formation() Shao, Xingxing Liu, Xin Qi, Hai Cell Insight Research Article Germinal center is a transient lymphoid tissue structure in which B cells undergo affinity maturation and differentiate into memory B cells and plasma cells. GC formation depends on B cell expression of BCL6, a master transcription regulator of the GC state. Bcl6 expression is under elaborate control by external signals. HES1 plays important roles in T-cell lineage commitment, although little is known about its potential roles in GC formation. Here we report that B-cell-specific HES1 deletion causes a significant increase in GC formation, leading to increased production of plasma cells. We further provide evidence that HES1 inhibits BCL6 expression in a bHLH domain-dependent manner. Our study suggests a new layer of regulation of GC initiation mediated by HES1 and, by inference, Notch signals in vivo. Elsevier 2023-01-28 /pmc/articles/PMC10134198/ /pubmed/37193067 http://dx.doi.org/10.1016/j.cellin.2023.100078 Text en © 2023 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Article
Shao, Xingxing
Liu, Xin
Qi, Hai
A role for Hes1 in constraining germinal center B cell formation()
title A role for Hes1 in constraining germinal center B cell formation()
title_full A role for Hes1 in constraining germinal center B cell formation()
title_fullStr A role for Hes1 in constraining germinal center B cell formation()
title_full_unstemmed A role for Hes1 in constraining germinal center B cell formation()
title_short A role for Hes1 in constraining germinal center B cell formation()
title_sort role for hes1 in constraining germinal center b cell formation()
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10134198/
https://www.ncbi.nlm.nih.gov/pubmed/37193067
http://dx.doi.org/10.1016/j.cellin.2023.100078
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