Literature DB >> 11809735

CD23 defines two distinct subsets of immature B cells which differ in their responses to T cell help signals.

James B Chung1, Richard A Sater, Michele L Fields, Jan Erikson, John G Monroe.   

Abstract

Transitional immature B cells undergo apoptosis and fail to proliferate in response to BCR cross-linking, thus representing a target for negative selection of potentially autoreactive B cells in vivo. In agreement with recent reports, transitional B cells were divided into developmentally contiguous subsets based on their surface expression of CD23. When transferred, CD23(+) transitional B cells readily localized to the splenic follicles and the outer PALS. Compared with CD23(-) transitional B cells, CD23(+) transitional B cells proliferated more vigorously and were rescued from BCR-induced apoptosis to a greater degree, by T cell help signals. However, both CD23(-) and CD23(+) transitional B cells failed to up-regulate CD86 (B7-2) in response to BCR ligation. These findings demonstrate that phenotypically defined subsets within the transitional B cell population are functionally distinct. Specifically, responsiveness to T cell help is a late acquisition corresponding to the stage when the B cells gain access to peripheral compartments enriched in antigen and activated T cells. The failure of transitional B cells to up-regulate CD86 to BCR-mediated stimulation suggests a unique interaction between transitional B cells and T cells with implications for tolerance in the T cell compartment.

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Year:  2002        PMID: 11809735     DOI: 10.1093/intimm/14.2.157

Source DB:  PubMed          Journal:  Int Immunol        ISSN: 0953-8178            Impact factor:   4.823


  26 in total

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Authors:  Novica M Milićević; Klaus Nohroudi; Zivana Milićević; Hans-Juergen Hedrich; Jürgen Westermann
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Review 3.  Characterization of splenic CD21hi T2 B cells.

Authors:  Shilpi Verma; Thomas J Waldschmidt
Journal:  Immunol Res       Date:  2007       Impact factor: 2.829

Review 4.  Signaling by the tumor necrosis factor receptor superfamily in B-cell biology and disease.

Authors:  Robert C Rickert; Julia Jellusova; Ana V Miletic
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5.  Notch1 is an important mediator for enhancing of B-cell activation and antibody secretion by Notch ligand.

Authors:  Jung-Ah Kang; Woo-Seok Kim; Sung-Gyoo Park
Journal:  Immunology       Date:  2014-12       Impact factor: 7.397

6.  Aiolos Overexpression in Systemic Lupus Erythematosus B Cell Subtypes and BAFF-Induced Memory B Cell Differentiation Are Reduced by CC-220 Modulation of Cereblon Activity.

Authors:  Yumi Nakayama; Jolanta Kosek; Lori Capone; Eun Mi Hur; Peter H Schafer; Garth E Ringheim
Journal:  J Immunol       Date:  2017-08-28       Impact factor: 5.422

Review 7.  The Plasticity of Newly Formed B Cells.

Authors:  Natalia V Giltiay; Daniela Giordano; Edward A Clark
Journal:  J Immunol       Date:  2019-12-15       Impact factor: 5.422

8.  Transitional B cells exhibit a B cell receptor-specific nuclear defect in gene transcription.

Authors:  Sarah F Andrews; David J Rawlings
Journal:  J Immunol       Date:  2009-03-01       Impact factor: 5.422

9.  Prolactin alters the mechanisms of B cell tolerance induction.

Authors:  Subhrajit Saha; Juana Gonzalez; Gabriel Rosenfeld; Harold Keiser; Elena Peeva
Journal:  Arthritis Rheum       Date:  2009-06

10.  Censoring of self-reactive B cells by follicular dendritic cell-displayed self-antigen.

Authors:  Irene W Yau; Matthew H Cato; Julia Jellusova; Tatiana Hurtado de Mendoza; Robert Brink; Robert C Rickert
Journal:  J Immunol       Date:  2013-07-01       Impact factor: 5.422

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