title: CD23 can negatively regulate B-cell receptor signaling.
abstract: CD23 has been implicated as a negative regulator of IgE and IgG antibody responses. However, whether CD23 has any role in B-cell activation remains unclear. We examined the expression of CD23 in different subsets of peripheral B cells and the impact of CD23 expression on the early events of B-cell receptor (BCR) activation using CD23 knockout (KO) mice. We found that in addition to marginal zone B cells, mature follicular B cells significantly down regulate the surface expression level of CD23 after undergoing isotype switch and memory B-cell differentiation. Upon stimulation with membrane-associated antigen, CD23 KO causes significant increases in the area of B cells contacting the antigen-presenting membrane and the magnitude of BCR clustering. This enhanced cell spreading and BCR clustering is concurrent with increases in the levels of phosphorylation of tyrosine and Btk, as well as the levels of F-actin and phosphorylated Wiskott Aldrich syndrome protein, an actin nucleation promoting factor, in the contract zone of CD23 KO B cells. These results reveal a role of CD23 in the negative regulation of BCR signaling in the absence of IgE immune complex and suggest that CD23 down-regulates BCR signaling by influencing actin-mediated BCR clustering and B-cell morphological changes.
authors.affiliation: Department of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan 430030, China.
authors.forename: Chaohong
authors.initials: C
authors.lastname: Liu
authors.affiliation: Department of Microbiology &Immunology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
authors.forename: Katharina
authors.initials: K
authors.lastname: Richard
authors.affiliation: Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA.
authors.forename: Melvin
authors.initials: M
authors.lastname: Wiggins
authors.affiliation: Department of Veterinary Medicine, University of Maryland, College Park, MD 20742, USA.
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Zhu
authors.affiliation: Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23298, USA.
authors.forename: Daniel H
authors.initials: DH
authors.lastname: Conrad
authors.affiliation: Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA.
authors.forename: Wenxia
authors.initials: W
authors.lastname: Song
mesh_terms: D000199:Actins / Q000276:immunology / Q000378:metabolism; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D017578:Immunoglobulin Class Switching / Q000235:genetics / Q000276:immunology; D007156:Immunologic Memory / Q000235:genetics / Q000276:immunology; D008213:Lymphocyte Activation / Q000235:genetics / Q000276:immunology; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010766:Phosphorylation / Q000276:immunology; D011947:Receptors, Antigen, B-Cell / Q000276:immunology* / Q000378:metabolism; D017455:Receptors, IgE / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology*; D051316:Wiskott-Aldrich Syndrome Protein / Q000276:immunology / Q000378:metabolism
chemical_list: D000199:Actins; D011947:Receptors, Antigen, B-Cell; D017455:Receptors, IgE; C495768:Was protein, mouse; D051316:Wiskott-Aldrich Syndrome Protein