| First Author | Saitoh SI | Year | 2019 |
| Journal | Int Immunol | Volume | 31 |
| Issue | 4 | Pages | 225-237 |
| PubMed ID | 30753473 | Mgi Jnum | J:273314 |
| Mgi Id | MGI:6286635 | Doi | 10.1093/intimm/dxy084 |
| Citation | Saitoh SI, et al. (2019) ADP-ribosylation factor-like 8b is required for the development of mouse models of systemic lupus erythematosus. Int Immunol 31(4):225-237 |
| abstractText | Toll-like receptor 7 (TLR7) and type I interferons (IFN-1) are essential for the development of systemic lupus erythematosus (SLE) models such as BXSB.Yaa and 2,6,10,14-tetramethyl-pentadecane (TMPD)-induced experimental lupus. However, the mechanism underlying the development of SLE remains undefined. We report a requirement for ADP-ribosylation factor-like 8b (Arl8b) for TLR7-dependent IFN-1 production in plasmacytoid dendritic cells (pDCs). We analyzed whether Arl8b plays a role in two SLE models by comparing wild-type and Arl8b-deficient Arl8b GeneTrap (Arl8bGt/Gt) mice. We found that BXSB.Yaa Arl8bGt/Gt mice showed none of the abnormalities characterized in BXSB.Yaa mice. TMPD treatment of Arl8bGt/Gt mice significantly inhibited the development of SLE. pDCs were required for TMPD-induced peritonitis. Our data demonstrate that Arl8b contributes to disease pathogenesis in two SLE models via IFN-1-dependent and -independent mechanisms and suggest that Arl8b is an attractive new target for therapeutic intervention in SLE. |
