Journal of cellular biochemistry · 2016
STAT5A Modulates Chemokine Receptor CCR6 Expression and Enhances Pre-B Cell Growth in a CCL20-Dependent Manner.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Tsuruyama Tatsuaki, Hiratsuka Takuya, Aini Wulamujiang, Nakamura Takuro
Аннотация
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.
Предметные рубрики MeSH
AnimalsApoptosisBlotting, WesternCell ProliferationCells, CulturedChemokine CCL20CytokinesHumansImmunoenzyme TechniquesInflammationLymphoma, B-CellMicePhosphorylationPrecursor Cells, B-LymphoidRNA, MessengerReal-Time Polymerase Chain ReactionReceptors, CCR6Reverse Transcriptase Polymerase Chain ReactionSTAT5 Transcription FactorSignal Transduction