| First Author | Lee MR | Year | 2011 |
| Journal | Biochem Biophys Res Commun | Volume | 410 |
| Issue | 3 | Pages | 602-7 |
| PubMed ID | 21684254 | Mgi Jnum | J:174949 |
| Mgi Id | MGI:5141552 | Doi | 10.1016/j.bbrc.2011.06.035 |
| Citation | Lee MR, et al. (2011) iNOS potentiates mouse Ig isotype switching through AID expression. Biochem Biophys Res Commun 410(3):602-7 |
| abstractText | The IgA antibody plays an important role in protecting mucosal surfaces against pathogens. It has recently been shown that nitric oxide (NO) plays a critical role in mouse IgA synthesis. In the present study, we further characterized inducible-nitric oxide synthase-deficient (iNOS(-/-)) mice in the context of Ig expression. The amount of IgA in fecal pellets was substantially diminished in iNOS(-/-) mice and was paralleled by a decrease in IgA production by Peyer's patch cells. Interestingly, the amount of all IgG subisotypes, as well as IgA, was substantially diminished in sera and in cultured spleen B cells from iNOS(-/-) mice. Moreover, the synthesis of TGF-beta1-inducible IgA and IgG2b in iNOS(-/-) mice was also lower than that in WT mice. However, levels of Ig germ-line transcripts, and expression of TGF-beta receptor type II (TbetaRII) and BAFF/APRIL, were comparable between iNOS(-/-) and WT mice. Expression of activation-induced cytidine deaminase (AID) was diminished in iNOS(-/-) B cells, but restored by a NO donor, SNAP. These results indicate that iNOS regulates Ig isotype switching events at the level of AID gene expression. |
