科研人員通過研究健康人群的免疫系統(tǒng)發(fā)現(xiàn),，有兩種細胞的相互作用可能有助于解釋為什么機體的自然防御系統(tǒng)未能識別和戰(zhàn)勝腫瘤,。該研究成果發(fā)表在新一期的《美國國家科學(xué)院院刊》上,。“這無疑為治療癌癥和開發(fā)新的靶向藥物提供了新的方向”,，該試驗的領(lǐng)導(dǎo)者倫敦大學(xué)國王學(xué)院免疫學(xué)家LeonieTaams說,。
調(diào)節(jié)性T細胞能保持免疫系統(tǒng)的穩(wěn)定,，主要控制引起炎癥的巨噬細胞,，炎癥是機體對付感染的第一反應(yīng),。正是由于調(diào)節(jié)性T細胞阻止了殺傷性T細胞對腫瘤發(fā)動的襲擊，它們也能“幽禁”巨噬細胞從而抑制炎癥和機體對腫瘤的“監(jiān)視”,。調(diào)節(jié)性T細胞可迷惑免疫系統(tǒng),，即使腫瘤發(fā)生也裝作若無其事?？茖W(xué)家早就知道細菌等微生物能刺激巨噬細胞,，但其功能如何被封閉依然是個謎。
雖然該研究在健康人群中進行,，但對于治療癌癥也具有一定的意義,，Taams認為，調(diào)節(jié)性T細胞確實是在發(fā)揮作用,，但不是在正確的時間和地點,。因此，從腫瘤組織中移除調(diào)節(jié)性T細胞或許對治療更有效,。（醫(yī)藥經(jīng)濟報）
原始出處:
Published online before print October 17, 2007, 10.1073/pnas.0708426104
PNAS | October 23, 2007 | vol. 104 | no. 43 | 17034-17039
Optimal induction of T helper 17 cells in humans requires T cell receptor ligation in the context of Toll-like receptor-activated monocytes
Hayley G. Evans*, Tesha Suddason, Ian Jackson, Leonie S. Taams*,, and Graham M. Lord,,,¶
Departments of *Immunobiology and Nephrology and Transplantation, King's College London, London SE1 9RT, United Kingdom; Harvard School of Public Health, Harvard University, Boston, MA 02115; and ¶National Institute for Health Research Biomedical Research Centre, Guy's and St. Thomas' Hospital and King's College London, London SE1 9RT, United Kingdom
Communicated by Laurie H. Glimcher, Harvard Medical School, Boston, MA, September 5, 2007 (received for review August 1, 2007)
Recently, a new lineage of CD4+ T cells has been described in the mouse that specifically secretes IL-17 [T helper (Th) 17]. This discovery has led to a revision of the hypothesis that many autoimmune diseases are predominantly a Th1 phenomenon and may instead be critically dependent on the presence of Th17 cells. Murine Th17 cells differentiate from naïve T cell precursors in the presence of TGF- and IL-6 or IL-21. However, given their putative importance in human autoimmunity, very little is known about the pathways that control the expression of IL-17 in humans. Here we show that the factors that determine the expression of IL-17 in human CD4+ T cells are completely different from mice. IL-6 and IL-21 were unable to induce IL-17 expression in either naïve or effector T cells, and TGF- actually inhibited IL-17 expression. The expression of IL-17 was maximally induced from precommitted precursors present in human peripheral blood by cell–cell contact with Toll-like receptor-activated monocytes in the context of T cell receptor ligation. Furthermore, unlike IFN-, IL-17 expression was not suppressed by the presence of FOXP3+ regulatory CD4+ T cells. Taken together, these data indicate that human and mouse Th17 cells have important biological differences that may be of critical importance in the development of therapeutic interventions in diseases characterized by aberrant T cell polarization.
autoimmunity | IL-17 | T lymphocytes
