Deficiency in TNFRSF13B (TACI) expands T-follicular helper and germinal center B cells via increased ICOS-ligand expression but impairs plasma cell survival

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 109; no. 38; pp. 15401 - 15406
• Main Authors: Ou, Xijun, Xu, Shengli, Lam, Kong-Peng
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences 18.09.2012; National Acad Sciences
• Subjects: Animals; Antibodies; Antigens; Autoimmunity; B lymphocytes; B-Lymphocytes - cytology; B-Lymphocytes - immunology; Biological Sciences; Common variable immunodeficiency; Flow Cytometry - methods; Gene Expression Regulation; Germinal Center - immunology; Humans; Immune System; Inducible T-Cell Co-Stimulator Protein - metabolism; Ligands; Lymphoid tissue; Mice; Mice, Inbred C57BL; Mice, Transgenic; Mutation; Plasma; Plasma cells; Plasma Cells - cytology; Receptors, Tumor Necrosis Factor - biosynthesis; Rodents; Spleen; T cell receptors; T-Lymphocytes, Helper-Inducer - immunology; Transmembrane Activator and CAML Interactor Protein - biosynthesis; Transmembrane Activator and CAML Interactor Protein - genetics; Up regulation

Mutations in TNFRSF13B, better known as transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI), contribute to common variable immunodeficiency and autoimmunity in humans. How TACI regulates these two opposing conditions is unclear, however. TACI binds the cytokines BA...