| First Author | Tsuruyama T | Year | 2016 |
| Journal | J Cell Biochem | Volume | 117 |
| Issue | 11 | Pages | 2630-42 |
| PubMed ID | 27018255 | Mgi Jnum | J:259640 |
| Mgi Id | MGI:6148013 | Doi | 10.1002/jcb.25558 |
| Citation | Tsuruyama T, et al. (2016) STAT5A Modulates Chemokine Receptor CCR6 Expression and Enhances Pre-B Cell Growth in a CCL20-Dependent Manner. J Cell Biochem 117(11):2630-42 |
| abstractText | Signal transducer and activator of transcription 5A (STAT5A) contributes to B-cell responses to cytokines through suppressor of cytokine signaling (Socs) genes in innate immunity. However, its direct roles in B-cell responses to chemokines are poorly understood. In this study, we examined the role of STAT5A in the innate immune response. We found that STAT5A upregulated the transcription of C-C motif receptor 6 (Ccr6) to induce responses to its ligand, CCL20. STAT5A transcriptional activity proceeded through binding to the interferon-gamma activation site (GAS) element in the CCR6 promoter in the genome of pre-B cells. High levels of STAT5A and CCR6 increased CCL20-dependent colony growth of pre-B cells. In human B-lymphoblastic lymphoma with inflammation, STAT5A phosphorylation was correlated with CCR6 expression (P > 0.05 compared with that in cases without inflammation). In conclusion, our data supported our hypothesis that STAT5A enhanced the response of pre-B cells to CCL20 to promote their growth. J. Cell. Biochem. 117: 2630-2642, 2016. (c) 2016 Wiley Periodicals, Inc. |
