国产bbaaaaa片,成年美女黄网站色视频免费,成年黄大片,а天堂中文最新一区二区三区,成人精品视频一区二区三区尤物

首頁> 外文學(xué)位 >FoxP3+ Regulatory T Cell Fate in Inflamed Tissues.
【24h】

FoxP3+ Regulatory T Cell Fate in Inflamed Tissues.

機譯：炎癥組織中的FoxP3 +調(diào)節(jié)性T細胞命運。

獲取原文
獲取原文并翻譯 | 示例
  • 摘要
  • 著錄項
  • 相似文獻
  • 相關(guān)主題

摘要

Regulatory CD4+ T cells (Tregs), classically defined by expression of CD25 and the transcription factor FoxP3, are immunosuppressive sentinels that function under a variety of tissues and inflammatory milieu. Tregs express different transcriptional signatures within distinct anatomical locations. However, whether the modulation of Tregs is due to distinct anatomical locations or the type of inflammation within the tissue remains unknown. We sought to define factors that govern Treg modulation in differently inflamed skin, and in healthy and autoimmune pancreas compared to lymphoid tissues. Our data reveal three major observations in Treg accumulation and function in non-lymphoid tissues in disease and under different types of inflammation. 1) Treg accumulation in non-lymphoid tissues is drastically changed depending on the type of inflammatory milieu, which may lead to changes in Treg survival or development of autoimmune diabetes. Our skin model suggests that inflammatory changes in IL-23: IL-33 may be important in Treg accumulation and survival in tissues. In both the pancreas and skin, increased accumulation patterns correlated with a higher expression of surface CD25 on Tregs, a receptor implicated in Treg survival. Interestingly, CD25 upregulation was specific to the type of inflammatory milieu. 2) Surprisingly, gross changes in Treg transcriptional phenotype correlated more with anatomical location (skin and pancreas compared to LN) than the type of inflammation or disease state within the tissue. We identified a small number of novel transcriptional changes in Tregs associated with the diseased pancreas. 3) Inflammatory milieu directly affects Treg response to antigen in the skin. Only in inflammatory milieus that upregulated CD25 did the provision of antigen enhance local Treg proliferation. Thus, the magnitude of the Treg response in inflamed tissues is controlled at two inter-dependent levels: inflammatory signals that support the upregulation of the important Treg survival factor, CD25, and the antigen signals that drive local expansion. These results begin to reconcile some of the in vivo discrepancies about the modulation of Tregs in the non-lymphoid tissues during inflammation and autoimmune disease. Importantly, our studies may be used to advance immune therapies to govern Treg maintenance in different inflammatory and anatomical locations.
機譯：調(diào)節(jié)性CD4 + T細胞（Tregs），通常由CD25和轉(zhuǎn)錄因子FoxP3的表達來定義，是免疫抑制的前哨，在多種組織和炎癥環(huán)境下起作用。 Treg在不同的解剖位置表達不同的轉(zhuǎn)錄特征。然而，是否調(diào)節(jié)Tregs是由于不同的解剖學(xué)位置還是組織內(nèi)炎癥的類型所致。我們試圖定義與淋巴組織相比，在不同程度發(fā)炎的皮膚以及健康和自身免疫性胰腺中控制Treg調(diào)節(jié)的因素。我們的數(shù)據(jù)揭示了疾病和不同類型炎癥下非淋巴組織中Treg積累和功能的三個主要觀察結(jié)果。 1）根據(jù)炎性環(huán)境的類型，非淋巴組織中的Treg積累會發(fā)生巨大變化，這可能導(dǎo)致Treg存活率發(fā)生變化或自身免疫性糖尿病的發(fā)展。我們的皮膚模型表明IL-23：IL-33中的炎癥變化可能對組織中Treg的積累和存活很重要。在胰腺和皮膚中，積累的模式增加與Tregs上表面CD25的更高表達有關(guān)，Tregs是與Treg存活有關(guān)的受體。有趣的是，CD25上調(diào)是特定于炎癥環(huán)境的。 2）令人驚訝的是，Treg轉(zhuǎn)錄表型的總體變化與解剖位置（與LN相比，皮膚和胰腺）的關(guān)系大于組織內(nèi)炎癥或疾病狀態(tài)的類型。我們在與患病胰腺相關(guān)的Tregs中發(fā)現(xiàn)了少量新穎的轉(zhuǎn)錄變化。 3）炎癥環(huán)境直接影響Treg對皮膚抗原的反應(yīng)。僅在上調(diào)CD25的炎性環(huán)境中，抗原的提供才增強局部Treg增殖。因此，發(fā)炎組織中Treg反應(yīng)的強度控制在兩個相互依存的水平：支持重要Treg生存因子CD25上調(diào)的炎癥信號和驅(qū)動局部擴增的抗原信號。這些結(jié)果開始調(diào)和一些在炎癥和自身免疫性疾病期間非淋巴組織中Tregs調(diào)節(jié)的體內(nèi)差異。重要的是，我們的研究可用于推進免疫療法，以控制不同炎癥和解剖部位Treg的維持。

著錄項

  • 作者單位

    University of Rochester.;

  • 授予單位 University of Rochester.;
  • 學(xué)科 Microbiology.;Molecular biology.;Cellular biology.;Immunology.;Genetics.
  • 學(xué)位 Ph.D.
  • 年度 2016
  • 頁碼 176 p.
  • 總頁數(shù) 176
  • 原文格式 PDF
  • 正文語種 eng
  • 中圖分類
  • 關(guān)鍵詞

相似文獻

  • 外文文獻
  • 中文文獻
  • 專利
獲取原文

客服郵箱：kefu@zhangqiaokeyan.com

京公網(wǎng)安備：11010802029741號 ICP備案號：京ICP備15016152號-6 六維聯(lián)合信息科技 (北京) 有限公司?版權(quán)所有

  • 客服微信

  • 服務(wù)號