| First Author | Fujimoto M | Year | 1999 |
| Journal | Immunity | Volume | 11 |
| Issue | 2 | Pages | 191-200 |
| PubMed ID | 10485654 | Mgi Jnum | J:76973 |
| Mgi Id | MGI:2180692 | Doi | 10.1016/s1074-7613(00)80094-1 |
| Citation | Fujimoto M, et al. (1999) Modulation of B lymphocyte antigen receptor signal transduction by a CD19/CD22 regulatory loop. Immunity 11(2):191-200 |
| abstractText | CD19 and CD22 are B lymphocyte cell-surface molecules that positively and negatively regulate antigen receptor signal transduction, respectively. Biochemical studies with B cells from CD19-deficient and CD22-deficient mice indicated that these two regulatory molecules influenced each other's functions: CD22 expression negatively regulated CD19 tyrosine phosphorylation, while optimal CD22 function was dependent on CD19 expression. Functional CD19 and CD22 interactions were also assessed in vivo by generating CD19/CD22 double-deficient mice. Remarkably, the CD19 mutation was dominant to the CD22 mutation in most instances. B lymphocytes from CD19/CD22-deficient and CD19-deficient mice were functionally equivalent despite the negative influence normally provided by CD22 expression. These data collectively suggest that CD19 activates the CD22/SHP1 inhibitory pathway that then acts primarily on CD19. |
