Lactoferrin Combined with Retinoic Acid Stimulates B1 Cells to Express IgA Isotype and Gut-homing Molecules
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It is well established that TGF-β1 and retinoic acid (RA)cause IgA isotype switching in mice. We recently found thatlactoferrin (LF) also has an activity of IgA isotype switchingin spleen B cells. The present study explored the effect of LFon the Ig production by mouse peritoneal B cells. LF, likeTGF-β1, substantially increased IgA production in peritonealB1 cells but little in peritoneal B2 cells. In contrast, LF increasedIgG2b production in peritoneal B2 cells much morestrongly than in peritoneal B1 cells. LF in combination withRA further enhanced the IgA production and, interestingly,this enhancement was restricted to IgA isotype and B1 cells. Similarly, the combination of the two molecules also led toexpression of gut homing molecules α4β7 and CCR9 onperitoneal B1 cells, but not on peritoneal B2 cells. Thus,these results indicate that LF and RA can contribute to gutIgA response through stimulating IgA isotype switching andexpression of gut-homing molecules in peritoneal B1 cells.
Abstract
It is well established that TGF-β1 and retinoic acid (RA)cause IgA isotype switching in mice. We recently found thatlactoferrin (LF) also has an activity of IgA isotype switchingin spleen B cells. The present study explored the effect of LFon the Ig production by mouse peritoneal B cells. LF, likeTGF-β1, substantially increased IgA production in peritonealB1 cells but little in peritoneal B2 cells. In contrast, LF increasedIgG2b production in peritoneal B2 cells much morestrongly than in peritoneal B1 cells. LF in combination withRA further enhanced the IgA production and, interestingly,this enhancement was restricted to IgA isotype and B1 cells. Similarly, the combination of the two molecules also led toexpression of gut homing molecules α4β7 and CCR9 onperitoneal B1 cells, but not on peritoneal B2 cells. Thus,these results indicate that LF and RA can contribute to gutIgA response through stimulating IgA isotype switching andexpression of gut-homing molecules in peritoneal B1 cells.
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