|
ИСТИНА |
Войти в систему Регистрация |
Интеллектуальная Система Тематического Исследования НАукометрических данных |
||
Constitutive STAT5 phosphorylation is critical for interleukin-2 receptor alpha expression in human blood T lymphocytesстатья
Информация о цитировании статьи получена из
Web of Science
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 7 сентября 2017 г.
- Авторы: Mityushova E., Shatrova A., Zenin V., Marakhova I.
- Журнал: FEBS Journal
- Том: 280
- Номер: 1
- Год издания: 2013
- Издательство: Blackwell Publishing Inc.
- Местоположение издательства: United Kingdom
- Первая страница: 469
- Последняя страница: 470
- Аннотация: The interleukin-2 receptor alpha (IL-2Ralpha) in association with IL-2Rbeta and IL-2Rgammac forms a high affinity IL-2R that is important for normal T cell function and proliferation. Expression of the IL-2Ralpha gene by T cells is regulated mainly at the transcription level by antigen and cytokine. In primary human blood T cells we used pharmacological drugs to separate distinct signal pathways which are involved in IL-2Ralpha expression (assayed by flow cytometric analysis of CD25+ cells) and showed that the Src-dependent signalling (via TCR) preceeded the Jakdependent signalling (via IL-2R) during cell surface expression of CD25. Since recombined IL-2 was revealed to induce CD25 expression in competent (not in quiescent) T cells, the role of STAT5 signal delivered downstream of IL-2R was elucidated. Western blot analysis showed that STAT5 protein was unfosphorylated in quiescent lymphocytes. The tyrosine phosphorylation of STAT5 appeared only after 2 h of phytogemagglutinine (PHA) stimulation and high phosphorylation of STAT5 is observed during the next 48 h. In quiescent blood lymphocytes IL-2 induced short-term increase in STAT5 phosphorylation, whereas in the competent cells STAT5 phosphorylation was induced by IL-2 at 30 min and was kept at a high level during the next 48 h. WHI-P131, an inhibitor of Jak3 kinase, prevents STAT5 activation, cell surface expression of CD25 and lymphocyte proliferation. A correlation between alterations in tyrosine phosphorylation level of STAT5 and the expression of CD25 was established in T lymphocytes stimulated by PHA or IL-2. It is concluded that Jak3/STAT5 signalling via IL-2 receptor is nessesary to support the long-term expression of high-affinity receptor of IL-2 and optimal proliferation of primary T lymphocytes.
- Добавил в систему: Марахова Ирина Ильинична