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Updated: Jul 24, 2025

Evaluation of T Follicular Helper Cells and Germinal Center Response During Influenza A Virus Infection in Mice
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TACI and endogenous APRIL in B cell maturation

Yolanda Garcia-Carmona1, Miguel Fribourg2, Allison Sowa3

  • 1Division of Clinical Immunology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York City, NY 10029, USA; Marc and Jennifer Lipschultz Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York City, NY 10029, USA.

Clinical Immunology (Orlando, Fla.)
|July 8, 2023
PubMed

While many of the genes and molecular pathways in the germinal center B cell response which initiate protective antibody production are known, the contributions of individual molecular players in terminal B cell differentiation remain unclear. We have previously investigated how mutations in TACI gene, noted in about 10% of patients with common variable immunodeficiency, impair B cell differentiation and often, lead to lymphoid hyperplasia and autoimmunity. Unlike mouse B cells, human B cells express TACI-L (Long) and TACI-S (Short) isoforms, but only TACI-S promotes terminal B cell differentiation into plasma cells. Here we show that the expression of intracellular TACI-S increases with B cell activation, and colocalizes with BCMA and their ligand, APRIL. We show that the loss of APRIL impairs isotype class switch and leads to distinct metabolic and transcriptional changes. Our studies suggest that intracellular TACI-S and APRIL along with BCMA direct long-term PC differentiation and survival.

Keywords:
A proliferation inducing ligand (APRIL)BCMA (B cell maturation antigen)Plasma cellTACI (transmembrane activator and CAML interactor)

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