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(Received for publication, January 29, 1997)
From the Geneva Biomedical Research Institute, GlaxoWellcome
Research and Development, Immunology Department, 14, Chemin des Aulx,
CH-1228 Plan les Ouates, Geneva, Switzerland and
Immunoglobulin (Ig) E production by B cells
requires two primary signals provided by T cells, interleukin (IL)-4 or
IL-13 and CD40 ligand (CD40L). In addition, costimulatory signals, such as CD23-CD21 interaction, contribute further ensuring a selective control over this production. Recently, CD28, expressed on T cells, has
been reported to be involved in this process. The CD28 ligands, CD80
(B7-1) and CD86 (B7-2), are expressed on human tonsillar B cells, and
their expression is up-regulated by IL-4, IL-13, and/or an anti-CD40
monoclonal antibody (mAb). We have investigated whether signaling via
the B7 molecules affects IgE synthesis. Human B cells were stimulated
by IL-4 plus anti-CD40 mAb in the presence of different anti-B7 mAbs.
Cross-linking of CD86 with IT2.2 potentiated IgE and IgG4 production
and
Volume 272, Number 25,
Issue of June 20, 1997
pp. 15613-15619
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
A FUNCTIONAL ROLE IN PROLIFERATION AND SELECTIVE DIFFERENTIATION
INTO IgE- AND IgG4-PRODUCING CELLS
and
GlaxoWellcome Medicines Research Centre, Immunopathology
Unit, Gunnels Wood Road, Stevenage, Hertfordshire,
SG1 2NY, United Kingdom
transcripts expression. The production of the other isotypes
was not modulated. Conversely, the anti-CD80 and the other anti-CD86
mAbs tested had no effect. The increase of IgE and IgG4 production
induced by IT2.2 was accompanied by an increase in proliferation, in
cell surface density of CD23, and in CD23 binding to CD21-expressing B
cells. In contrast, the expression of other B cell surface molecules
such as CD11a, CD30, and CD58 remained unaffected. Since IT2.2 favors
CD23-CD21 pairing, we tested whether blocking this interaction affected
IT2.2-increased IgE production. The neutralizing anti-CD23 mAb, Mab 25, caused a dose-dependent inhibition of the effect of IT2.2
on IgE synthesis. Finally, IT2.2 potentiation on B cell proliferation
and IgE production required the two primary signals, IL-4 and anti-CD40
mAb, since IT2.2 alone or in combination with only one of these stimuli
did not show any effect on B cells. This study is the first
demonstration of a signaling role for CD86. Together with IL-4 or IL-13
and CD40L, CD86 favors CD23-CD21 pairing and consequently functions as
a selective and potent costimulus for human IgE and IgG4 synthesis.
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