| First Author | Lombard-Vadnais F | Year | 2023 |
| Journal | iScience | Volume | 26 |
| Issue | 1 | Pages | 105852 |
| PubMed ID | 36654860 | Mgi Jnum | J:332666 |
| Mgi Id | MGI:7428155 | Doi | 10.1016/j.isci.2022.105852 |
| Citation | Lombard-Vadnais F, et al. (2023) Activation-induced cytidine deaminase expression by thymic B cells promotes T-cell tolerance and limits autoimmunity. iScience 26(1):105852 |
| abstractText | Elimination of self-reactive T cells in the thymus is critical to establish T-cell tolerance. A growing body of evidence suggests a role for thymic B cells in the elimination of self-reactive thymocytes. To specifically address the role of thymic B cells in central tolerance, we investigated the phenotype of thymic B cells in various mouse strains, including non-obese diabetic (NOD) mice, a model of autoimmune diabetes. We noted that isotype switching of NOD thymic B cells is reduced as compared to other, autoimmune-resistant, mouse strains. To determine the impact of B cell isotype switching on thymocyte selection and tolerance, we generated NOD.AID(-/-) mice. Diabetes incidence was enhanced in these mice. Moreover, we observed reduced clonal deletion and a resulting increase in self-reactive CD4(+) T cells in NOD.AID(-/-) mice relative to NOD controls. Together, this study reveals that AID expression in thymic B cells contributes to T-cell tolerance. |
