Brain Acid-Soluble Protein 1 (BASP1) maintains germinal centers by regulating germinal center B cell survival.

Germinal centers (GCs) are specialized sites in lymphoid tissues where antigen-specific B cells undergo proliferation, affinity maturation, and differentiation into high-affinity memory B cells and long-lived plasma cells following immunization or infection. The specific signals and mechanisms that are involved in GC B cell initiation, maintenance, and differentiation are not completely understood. Here, we investigated the expression and function of brain acid-soluble protein 1 (BASP1). Previously, no specific role for BASP1 in adaptive immunity has been established. BASP1 expression is induced in early GC B cells and increases over time as the GC progresses. We demonstrate, using short hairpin RNA knockdown and conditional deletion in mice, that BASP1 functions to maintain GC responses by promoting GC B cell survival and reducing memory B cells, and increasing plasma cell output. Finally, BASP1 induces a unique transcriptional program in GC B cells, enriched for interferon-γ- and interleukin-12-responsive genes. Thus, BASP1 regulates the survival and transcriptome of GC B cells as well as alters the nature of the memory B cell subset and plasma cell generation.