Stimulation of the B cell receptor, CD86 (B7-2), and the β2-adrenergic receptor intrinsically modulates the level of IgG1 and IgE produced per B cell

Deborah J. Kasprowicz, Adam P. Kohm, Michael T. Berton, Andrezj J. Chruscinski, Arlene Sharpe, Virginia M. Sanders

Research output: Contribution to journalArticle

113 Scopus citations

Abstract

Our findings using B cells from either wild-type, CD86-deficient, or β2-adrenergic receptor (β2AR)-deficient mice suggest three mechanisms by which the level of IgG1 and IgE production can be increased on a per cell basis. Trinitrophenyl-specific B cells enriched from unimmunized mouse spleens were pre-exposed to Ag and/or the β2AR ligand terbutaline for 24 h before being activated by either a β2AR-negative Th2 cell clone or CD40 ligand/Sf9 cells and IL-4 in the presence or absence of an anti-CD86 Ab. Data suggest that the first mechanism involves a B cell receptor (BCR)-dependent up-regulation of CD86 expression that, when CD86 is stimulated, increases the amount of IgG1 and IgE produced in comparison to unstimulated cells. The second mechanism involves a BCR-and β2AR-dependent up-regulation of CD86 to a level higher than that induced by stimulation of either receptor alone that, when CD86 is stimulated, further increases the amount of IgG1 and IgE produced. The third mechanism is BCR-independent and involves a β2AR- dependent increase in the ability of a B cell to respond to IL-4. Flow cytometric and limiting dilution analyses suggest that the increase in IgG1 and IgE occurs independently from the isotype switching event. These findings suggest that the BCR, the β2AR, and CD86 are involved in regulating IL-4- dependent IgG1 and IgE production.

Original languageEnglish (US)
Pages (from-to)680-690
Number of pages11
JournalJournal of Immunology
Volume165
Issue number2
DOIs
StatePublished - Jul 15 2000

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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