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Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan
We show in this report a new regulatory role for IL-15 and IL-15R
in the development of B-1 cells and their differentiation into
IgA-producing cells. Mucosal IgA levels were found to be inhibited by
anti-IL-15 mAb treatment in vivo, but enhanced by administration of
rIL-15, while serum IgA levels remained unaffected. Mucosal B-1 cells
preferentially proliferated in response to IL-15 in vitro. When mucosal
B-1 and B-2 cells were separated into surface
(s)IgM+sIgA- and
sIgM-sIgA+ fractions, IL-15R-specific mRNA was
found to be predominant in both sIgM+sIgA- and
sIgM-sIgA+ B-1 cells at a much higher level
than B-2 cells. Further, incubation of these different subsets of B-1
and B-2 cells with IL-15 resulted in greater enhancement of the
corresponding receptor expression by B-1 subset when compared with B-2
fraction. Interestingly, de novo isolated
sIgM+sIgA- B-1, but not
sIgM+sIgA- B-2, cells were already
class-switched cells because the germline C
transcript was detected
and was then further enhanced by IL-15. IL-15 also supported
differentiation of both sIgM+sIgA- and
sIgM-sIgA+ B-1 cells into IgA-producing cells.
Taken together, these findings suggest that IL-15 is a critically
important cytokine for the differentiation of both
sIgM+,IgA- and
sIgM-sIgA+ B-1 cells expressing IL-15R into
IgA-producing cells in mucosal tissues.
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