| First Author | Stump M | Year | 2023 |
| Journal | Am J Physiol Regul Integr Comp Physiol | Volume | 324 |
| Issue | 2 | Pages | R161-R170 |
| PubMed ID | 36534590 | Mgi Jnum | J:340376 |
| Mgi Id | MGI:7439742 | Doi | 10.1152/ajpregu.00243.2022 |
| Citation | Stump M, et al. (2023) T cell-specific deficiency in BBSome component BBS1 interferes with selective immune responses. Am J Physiol Regul Integr Comp Physiol 324(2):R161-R170 |
| abstractText | Bsardet Biedl syndrome (BBS) is a genetic condition associated with various clinical features including cutaneous disorders and certain autoimmune and inflammatory diseases pointing to a potential role of BBS proteins in the regulation of immune function. BBS1 protein, which is a key component of the BBSome, a protein complex involved in the regulation of cilia function and other cellular processes, has been implicated in the immune synapse assembly by promoting the centrosome polarization to the antigen-presenting cells. Here, we assessed the effect of disrupting the BBSome, through Bbs1 gene deletion, in T cells. Interestingly, mice lacking the Bbs1 gene specifically in T cells (T-BBS1(-/-)) displayed normal body weight, adiposity, and glucose handling, but have smaller spleens. However, T-BBS1(-/-) mice had no change in the proportion and absolute number of B cells and T cells in the spleen and lymph nodes. There was also no alteration in the CD4/CD8 lineage commitment or survival in the thymus of T-BBS1(-/-) mice. On the other hand, T-BBS1(-/-) mice treated with Imiquimod dermally exhibited a significantly higher percentage of CD3-positive splenocytes that was due to CD4 but not CD8 T cell predominance. Notably, we found that T-BBS1(-/-) mice had significantly decreased wound closure, an effect that was more pronounced in males indicating that the BBSome plays an important role in T cell-mediated skin repair. Together, these findings implicate the BBSome in the regulation of selective functions of T cells. |
