| First Author | Zhang C | Year | 2016 |
| Journal | Immunity | Volume | 44 |
| Issue | 4 | Pages | 913-923 |
| PubMed ID | 27096320 | Mgi Jnum | J:258667 |
| Mgi Id | MGI:6140582 | Doi | 10.1016/j.immuni.2016.04.003 |
| Citation | Zhang C, et al. (2016) CD5 Binds to Interleukin-6 and Induces a Feed-Forward Loop with the Transcription Factor STAT3 in B Cells to Promote Cancer. Immunity 44(4):913-923 |
| abstractText | The participation of a specific subset of B cells and how they are regulated in cancer is unclear. Here, we demonstrate that the proportion of CD5(+) relative to interleukin-6 receptor alpha (IL-6Ralpha)-expressing B cells was greatly increased in tumors. CD5(+) B cells responded to IL-6 in the absence of IL-6Ralpha. IL-6 directly bound to CD5, leading to activation of the transcription factor STAT3 via gp130 and its downstream kinase JAK2. STAT3 upregulated CD5 expression, thereby forming a feed-forward loop in the B cells. In mouse tumor models, CD5(+) but not CD5(-) B cells promoted tumor growth. CD5(+) B cells also showed activation of STAT3 in multiple types of human tumor tissues. Thus, our findings demonstrate a critical role of CD5(+) B cells in promoting cancer. |
