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*
Department of Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan;
Department of Internal Medicine II, Chiba University School of Medicine, Chiba, Japan;
AgResearch, Ruakura, Hamilton, New Zealand; and
National Institutes of Diabetes, Digestive, and Kidney Diseases, Bethesda, MD
IL-5 stimulation of CD38-activated murine splenic B cells induces
µ-
1 CSR at the DNA level leading to a high level of IgG1
production. Further addition of IL-4 in the system enhances
IL-5-dependent µ-1 CSR. Although some of the postreceptor
signaling events initiated by IL-5 in activated B cells have been
characterized, the involvement of Stat in IL-5 signaling has not been
thoroughly evaluated. In this study, we examined the activation of
Stat5 and activation-induced cytidine deaminase (AID) in CD38-activated
murine splenic B cells by IL-5. The role of Stat5a and Stat5b in
IL-5-induced µ-1 CSR and also IgG1 and IgM production was
documented, as IL-5 does not act on CD38-stimulated splenic B cells
from Stat5a-/- and Stat5b-/- mice.
Expression levels of CD38-induced germline 1 transcripts and AID in
Stat5a-/- and Stat5b-/- B cells upon IL-5
stimulation were comparable to those of wild-type B cells. The impaired
µ-1 CSR by Stat5b-/- B cells, but not by
Stat5a-/- B cells, was rescued in part by IL-4, as the
addition of IL-4 to the culture of CD38- and IL-5-stimulated B cells
induced µ-1 CSR leading to IgG1 production. Analysis of cell
division cycle number of wild-type B cells revealed that µ-1 CSR
was observed after five or six cell divisions. Stat5a-/-
and Stat5b-/- B cells showed similar cell division
cycles, but they did not undergo µ-1 CSR. Our data support the
notion that both Stat5a and Stat5b are essential for IL-5-dependent
µ-1 CSR and Ig secretion; however, their major target may not be
AID. Stat5a and Stat5b are not redundant, but rather are at least
partially distinctive in their function.
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