| First Author | Khoenkhoen S | Year | 2022 |
| Journal | Front Immunol | Volume | 13 |
| Pages | 1000755 | PubMed ID | 36341341 |
| Mgi Jnum | J:333411 | Mgi Id | MGI:7383592 |
| Doi | 10.3389/fimmu.2022.1000755 | Citation | Khoenkhoen S, et al. (2022) IkappaBNS expression in B cells is dispensable for IgG responses to T cell-dependent antigens. Front Immunol 13:1000755 |
| abstractText | Mice lacking the atypical inhibitory kappa B (IkappaB) protein, IkappaBNS, a regulator of the NF-kappaB pathway encoded by the <i>nfkbid</i> gene, display impaired antibody responses to both T cell-independent (TI) and T cell-dependent (TD) antigens. To better understand the basis of these defects, we crossed mice carrying floxed <i>nfkbid</i> alleles with mice expressing Cre under the transcriptional control of the <i>Cd79a</i> gene to create mice that lacked IkappaBNS expression only in B cells. Analyses of these conditional knock-out mice revealed intact CD4<sup>+</sup> and CD8<sup>+</sup> T cell populations, including preserved frequencies of FoxP3<sup>+</sup> regulatory T cells, which are known to be reduced in IkappaBNS knock-out mice. Like IkappaBNS knock-out mice, mice with conditional IkappaBNS ablation in B cells displayed defective IgM responses to TI antigens and a severe reduction in peritoneal B-1a cells. However, in contrast to mice lacking IkappaBNS altogether, the conditional IkappaBNS knock-out mice responded well to TD antigens compared to the control mice, with potent IgG responses following immunization with the viral antigen, rSFV-betaGal or the widely used hapten-protein model antigen, NP-CGG. Furthermore, B cell intrinsic IkappaBNS expression was dispensable for germinal center (GC) formation and T follicular helper cell responses to NP-CGG immunization. The results presented here suggest that the defect in antibody responses to TD antigens observed in IkappaBNS knock-out mice results from a B cell extrinsic defect. |
