| First Author | Fang Y | Year | 2021 |
| Journal | Eur J Immunol | Volume | 51 |
| Issue | 1 | Pages | 103-114 |
| PubMed ID | 32652569 | Mgi Jnum | J:302237 |
| Mgi Id | MGI:6507796 | Doi | 10.1002/eji.202048640 |
| Citation | Fang Y, et al. (2021) The E3 ubiquitin ligase Itch deficiency promotes antigen-driven B-cell responses in mice. Eur J Immunol 51(1):103-114 |
| abstractText | Deficiency of Itch, an E3 ubiquitin ligase, usually induced severe systemic and progressive autoimmune disease. The Itch function is well studied in T cells but not in B cells. We hypothesize that B-cell-specific Itch deficiency promoted antigen-induced B-cell activation and antibody-expressing plasma cell (PC) production. We found that unlike Itch KO, Itch cKO (CD19(cre) Itch(f/f) ) mice did not demonstrated a significant increase in the sizes of spleens and LNs, antibody level, and base mutation of antibody gene. However, in line with the fact that Itch expression decreased in GC B cells, PCs, and plasmablast (PB)-like SP 2/0 cells, Itch deficiency promoted B-cell activation and antibody production induced by antigens including lipopolysaccharide (LPS) and sheep red blood cells (SRBCs). Mechanistically, we found that Itch deficiency promotes antigen-induced cytokine production because Itch controls the proteins (e.g., eIF3a, eIF3c, eIF3h) with translation initiation factor activity. Altogether, our data suggest that Itch deficiency promotes antigen-driven B-cell response. This may provide hints for Itch-targeted treatment of patients with autoimmune disease. |
