International Immunology, Vol 9, 1463-1473, Copyright © 1997 by Oxford University Press
M Baba, Y Kikuchi, S Mori, H Kimoto, S Inui, N Sakaguchi, J Inoue, T Yamamoto, T Takemori, M Howard and K Takatsu
The germinal center (GC) develops in secondary lymphoid tissues in response
to thymus-dependent (TD) antigens. To investigate the molecular mechanism
of B cell differentiation in GC, we enriched GC B cells from spleen of TD
antigen-immunized wild-type and X-linked immunodeficient (XID) mice, and
examined the differentiation of GC B cells into antigen-specific IgG1
antibody-forming cells (AFC) in response to anti-CD40 mAb and cytokines. A
significant proportion of freshly purified GC B cells expressed receptors
for IL-4 and IL-5. Anti- CD40 mAb sustained the viability of GC B cells and
IL-4 co-operated with anti-CD40 mAb for further enhancement of the cell
viability. Anti- CD40 mAb and IL-4 were essential for inducing
differentiation of GC B cells into antigen-specific IgG1-AFC and IL-5
efficiently enhanced their differentiation. GC B cells with the xid
mutation responded for proliferation to CD40 ligation to a lesser extent
and for the IgG1-AFC response to anti-CD40 mAb together with IL-4, but they
showed impaired responsiveness to IL-5, regardless of enhanced expression
of IL-5R in response to anti-CD40 mAb and IL-4. These results suggest that
anti- CD40 mAb, IL-4 and IL-5 play a critical role in the differentiation
of mouse GC B cells. The GC B cells from XID mice show a functional defect
with respect to IL-5-mediated differentiation.
ARTICLES
Mouse germinal center B cells with the xid mutation retain responsiveness to antimouse CD40 antibodies but diminish IL-5 responsiveness
Department of Immunology, University of Tokyo, Japan.
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