| First Author | Guo B | Year | 2013 |
| Journal | J Immunol | Volume | 191 |
| Issue | 2 | Pages | 670-7 |
| PubMed ID | 23776171 | Mgi Jnum | J:205452 |
| Mgi Id | MGI:5544883 | Doi | 10.4049/jimmunol.1203211 |
| Citation | Guo B, et al. (2013) IL-4 upregulates Igalpha and Igbeta protein, resulting in augmented IgM maturation and B cell receptor-triggered B cell activation. J Immunol 191(2):670-7 |
| abstractText | IL-4 is critical for optimal B cell activation and germinal center B cell expansion in T-dependent immune responses; however, the underlying mechanism remains elusive. In the current study, we found that primary B cells express little Igalpha and Igbeta protein despite substantial levels of mRNA. IL-4 markedly upregulates Igalpha and Igbeta protein expression that requires STAT6. Elevated Igalpha and Igbeta protein form heterodimers that associate with IgM and significantly promote IgM maturation and surface IgM expression, resulting in amplified BCR-initiated signaling that is Lyn dependent. In vivo, we found that pregerminal center B cells express upregulated Igalpha, Igbeta, and surface IgM expression, in conjunction with elevated BCR-triggered phosphorylated ERK ex vivo, that are dependent on IL-4 and reversed by in vivo administration of neutralizing anti-IL-4 Ab. Thus, this study elucidates a novel mechanism for cross-talk between the IL-4 and BCRs that programs enhancement of subsequent BCR signaling. |
