STAT5A Modulates Chemokine Receptor CCR6 Expression and Enhances Pre‐B Cell Growth in a CCL20‐Dependent Manner
STAT5A Modulates Chemokine Receptor CCR6 Expression and Enhances Pre‐B Cell Growth in a CCL20‐Dependent Manner
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DOI:
10.1002/jcb.25558
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发表时间:
2016-11
影响因子:
4
通讯作者:
T. Tsuruyama;T. Hiratsuka;Wulamujiang Aini;Takuro Nakamura
中科院分区:
文献类型:
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作者:
T. Tsuruyama;T. Hiratsuka;Wulamujiang Aini;Takuro Nakamura
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‐γ 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. © 2016 Wiley Periodicals, Inc.