Abstract
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.