T helper cell-induced CD23 (BLAST-2) expression: An activation marker for the high density fraction of human B cells

doi:10.1016/0090-1229(89)90105-0

Clinical Immunology and Immunopathology

Volume 53, Issue 1, October 1989, Pages 99-112

Clinical Immunology ...

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Abstract

We previously reported that the coculture of cloned, allospecific human T helper (T_h) cells with allogeneic B cells bearing the relevant major histocompatibility complex class II antigen induces expression of the B cell activation antigen CD23 (BLAST-2) on a fraction of the B cells. To determine if T_h cell-induced CD23 expression defines a distinct subset of human B cells, allospecific T_h cells were cultured with B cell fractions isolated on discontinuous Percoll gradients. Our results show that the majority of high density resting B cells, those bearing surface IgD and little of the 4F2 activation antigen, express high intensity CD23 after culture with relevant allospecific T_h cells. Essentially all of the low density, presumably in vivo-activated, B cell subpopulation and a fraction of the high density B cell pool remain CD23 negative after repeated culture with relevant allospecific T_h cells. We utilized the CD23 induction assay to investigate a potential synergistic effect in B cell activation mediated by T_h cell signaling and antigen analog-induced cross-linking of B cell surface Ig receptors. These studies show that phorbols known to result in PKC activation, one of the biochemical consequences of sIg-mediated B cell signaling, enhance both the intensity of CD23 expression and the percentage of cells expressing CD23 after allospecific T_h cell or IL-4 interaction with high density, but not low density B-cells. Finally, we show that while T_h-induced B cell activation, as measured by CD23 expression, is a property of high density B cells, induction of T_h cell proliferation is a property of the low density B cell population. These results suggest that the antigen-specific interaction between T_h cells and resting B cells may serve to activate the B cell in preference to the T cell.

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B-cell chronic lymphocytic leukemia cells express a surface membrane phenotype of activated, antigen-experienced B lymphocytes
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Citation Excerpt :
Furthermore, B-CLL cells can exhibit constitutive translocation of nuclear factor of activated T cells (NF-ATp)13 and phosphorylation of signal transducer and activator of transcription 1 (STAT-1) and STAT-3.14 Finally, most B-CLL cells express CD23, a cell surface marker acquired after B-cell activation.15-18 These findings suggest that certain B-CLL cells or their precursors may have been triggered and may have attempted to traverse the cell cycle, and may therefore not be resting or antigen-naive.
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Idiopathic anaphylaxis (IA), a type of anaphylaxis in which no external allergen can be identified, is a corticosteroid-responsive disease, that suggests that it may have an immunologic pathogenesis.
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Immunosenescence is characterized by an increase in autoantibody production. Because both T and B cell stimulation are key events for producing antibodies, we investigated early T and B cell activation by means of CD23 and CD40L (two very early activation antigens). PBMC from elderly humans (EH) were studied following culture with either medium, anti-CD3mAb, rIL-4, or PMA ± ionomycin. CD23 expression on elderly B cells after anti-CD3 challenge of PBMC, a reflect of T-dependent B cell activation, was clearly defective. Conversely, CD23 expression on EH B cells following activation with soluble factors as rIL-4 was preserved. CD40L expression was also impaired in EH T cells following anti-CD3 challenge. However, activation by means of PMA and/or ionomycin was preserved both in T cells (CD40L expression) and in B cells (CD23 expression). These results indicate that a defective T-dependent B cell activation related to defective T cell activation located between surface membrane and PKC/ionomycin function is an intrinsic characteristic of immunosenescence. We have not found intrinsic B-cell defects, and we conclude that the characteristically impaired early B cell activation in EH is mostly due to T cell defects.
HIV disease in children is associated with a selective decrease in CD23+ and CD62L+ B cells
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We have studied the causes of membrane CD23 (mCD23) hyperexpression in rheumatoid arthritis (RA). Modifying a previously developed in vitro system, we cultured RA and control peripheral blood (PB) mononuclear cells for 18 hr with medium, anti-CD3 monoclonal antibody (mAb), recombinant (r) IL-4, or phorbol mirystate acetate (PMA). After T cell depletion by rosetting, mCD23 was assessed by indirect immunofluorescence. RA PB B cells expressed mCD23 in a percentage significantly higher than controls unstimulated (16.7% vs. 6.6%) and after culture with anti-CD3-stimulated T cells (53% vs. 37.2%) or IL-4 (47% vs. 30%), but not after PMA (37.5% vs. 31%). We did not see differences in the percentages of resting B cells between RA and controls. Our results show an intrinsic RA PB B cell hyperesponsiveness to different T cell signals that might be mediated by in vivo priming through surface immunoglobulin.
Impaired Release of sCD23 by Activated B-Cells from RA Patients
1994, Clinical Immunology and Immunopathology
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Regular articleT helper cell-induced CD23 (BLAST-2) expression: An activation marker for the high density fraction of human B cells

Abstract

Cell. Immunol.

Cell

Annu. Rev. Immunol.

Nature (London)

Nature (London)

J. Exp. Med.

J. Immunol.

J. Immunol.

J. Immunol.

J. Immunol.

J. Exp. Med.

J. Mol. Cell. Immunol.

J. Immunol.

J. Exp. Med.

Nature (London)

J. Exp. Med.

J. Exp. Med.

Regular article
T helper cell-induced CD23 (BLAST-2) expression: An activation marker for the high density fraction of human B cells