| First Author | Cai Y | Year | 2019 |
| Journal | J Immunol | Volume | 202 |
| Issue | 2 | Pages | 407-420 |
| PubMed ID | 30541881 | Mgi Jnum | J:270100 |
| Mgi Id | MGI:6274813 | Doi | 10.4049/jimmunol.1800261 |
| Citation | Cai Y, et al. (2019) Deficiency of beta-Arrestin 2 in Dendritic Cells Contributes to Autoimmune Diseases. J Immunol 202(2):407-420 |
| abstractText | Altered migration and immune responses of dendritic cells (DCs) lead to inflammatory and autoimmune diseases. Our studies demonstrated that beta-arrestin 2 deficiency promoted migration and cytokine production of mouse bone marrow-derived DCs. We further found that beta-arrestin 2 directly interacted with Zbtb46, a DC-specific transcription factor. What's more, our results suggested that the interaction between beta-arrestin 2 and Zbtb46 might negatively regulate DC migration. Using RNA sequencing, we indicated that genes CD74, NR4A1, and ZFP36 might be the target genes regulated by the interaction between beta-arrestin 2 and Zbtb46. Mice with selective deficiency of beta-arrestin 2 in DCs developed severer experimental autoimmune encephalomyelitis with more DC infiltration in the CNS and increased IL-6 in serum. In the systemic lupus erythematosus mice model, Arrb2(fl/fl) Itgax-cre(+) mice were prone to exacerbation of lupus nephritis with a higher level of IL-6 and DC accumulation. Taken together, our study identified beta-arrestin 2 as a new regulator of DC migration and immune properties, providing new insights into the mechanisms underlying the development of autoimmune disease. |
