Abstract
IgA is a specific isotype required for mucosal immunity and is the most abundant Ab produced in vivo. Recently, several inductive signals for IgA class switch recombination have been identified; however, the molecular details of the action of these signals and the specific factors acting in B cells remain elusive. In this study, we show that combination of retinoic acid (RA) and TGF-beta1 with other factors induced a much higher frequency of IgA-switched cells than reported previously. In addition, IgA production is severely impaired in Runx2-Runx3 double-deficient mice. In Runx2-Runx3-deficient B cells, both RA- and TGF-beta1-dependent inductions of alpha germline transcription are completely blocked. These data suggest that Runx proteins play an essential role in IgA class switching acting downstream of RA and TGF-beta1 signaling.
Highlights
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Because Runx1 is essential for hematopoietic cell differentiation, all hemotopoietic lineages are absent in Runx12/2 mice; we focused on estimating the functions of Runx2 and Runx3 in IgA class switch recombination (CSR)
In Peyer’s patch (PP), high-affinity IgA is produced in a T cell-dependent manner
Summary
Requirement for Runx Proteins in IgA Class Switching Acting Downstream of TGF-b1 and Retinoic Acid Signaling These data suggest that Runx proteins play an essential role in IgA class switching acting downstream of RA and TGF-b1 signaling. We generated RAG2-deficient mice receiving runx2-runx3 doubledeficient fetal liver cells to analyze the functions of these factors in IgA class switching in vivo.
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