BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors

610 Receptors, Antigen, B-Cell B-Cell Activating Factor/immunology; B-Cell Activating Factor/metabolism; B-Cell Activation Factor Receptor/immunology; B-Cell Activation Factor Receptor/metabolism; Humans; Memory B Cells/immunology; Memory B Cells/metabolism; Phosphatidylinositol 3-Kinases/immunology; Phosphatidylinositol 3-Kinases/metabolism; Proto-Oncogene Proteins c-akt/immunology; Proto-Oncogene Proteins c-akt/metabolism; Receptors, Antigen, B-Cell/immunology; Receptors, Antigen, B-Cell/metabolism; BAFF; BAFFR; BCR; CP: Immunology; PI3K signaling; human memory B cells Phosphatidylinositol 3-Kinases 03 medical and health sciences Memory B Cells PI3K SIGNALING https://purl.org/becyt/ford/3.1 B-Cell Activating Factor Humans https://purl.org/becyt/ford/3 ddc:610 PI3K signaling ddc:610 0303 health sciences BAFFR HUMAN MEMORY B CELLS BCR 3. Good health CP: IMMUNOLOGY human memory B cells BAFF 610 Medizin und Gesundheit Proto-Oncogene Proteins c-akt B-Cell Activation Factor Receptor
DOI: 10.1016/j.celrep.2022.111019 Publication Date: 2022-06-28T20:15:18Z
ABSTRACT
Binding of BAFF to BAFFR activates in mature B cells PI3K/AKT signaling regulating protein synthesis, metabolic fitness, and survival. In humans, naive memory express the same levels BAFFR, but only seem survive without BAFF. Here, we show that changes expression genes migration, proliferation, growth, BAFF-induced activation requires direct interactions between cell antigen receptor (BCR) components CD79A CD79B is enhanced by AKT coactivator TCL1A. Compared cells, more surface BCRs, which interact better with than IgG or IgA, thus allowing stronger responses As ablation causes death independent signaling, seems act also as an intrinsic factor for
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