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Department of Patholoy, University of Massachusetts Medical School, Worcester, MA 01655; and
Department of Pediatrics, University of Colorado Health Sciences Center, Denver, CO 80262
Polyomavirus (PyV) infection elicits protective T cell-independent
(TI) IgG responses in T cell-deficient mice. The question addressed in
this report is whether CD40 signaling plays a role in this TI antiviral
IgG response. Because CD40 ligand (CD40L) can be expressed on numerous
cell types in addition to activated T cells, it is possible that cells
other than T cells provide CD40L to signal through CD40 on B cells and
hence positively influence the antiviral TI IgG responses. In this
study we show, by blocking CD40-CD40L interactions in vivo with
anti-CD40L Ab treatment in TCR ßx
-/- mice and
by using SCID mice reconstituted with CD40-/- B cells,
that the lack of CD40 signaling in B cells results in a 50% decrease
in TI IgG secreted in response to PyV. SCID mice reconstituted with
CD40L-/- B cells also responded to PyV infection with
diminished IgG secretion compared with that of SCID mice reconstituted
with wild-type B cells. This finding suggests that B cells may provide
the CD40L for CD40 signaling in the absence of T cell help during acute
virus infection. Our studies demonstrate that, although about half of
the TI IgG responses to PyV are independent of CD40-CD40L interactions,
these interactions occur in T cell-deficient mice and enhance antiviral
TI Ab responses.
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