Suppr超能文献

FoxO 转录因子:作为氧化应激相关疾病新型免疫细胞调节剂和治疗靶点的适用性。

FoxO Transcription Factors: Applicability as a Novel Immune Cell Regulators and Therapeutic Targets in Oxidative Stress-Related Diseases.

机构信息

Department of Life Science, Immunology Research Lab, BK21-plus Research Team for Bioactive Control Technology, College of Natural Sciences, Chosun University, Dong-gu, Gwangju 61452, Korea.

LKBio Inc., Chosun University Business Incubator (CUBI) Building, Dong-gu, Gwangju 61452, Korea.

出版信息

Int J Mol Sci. 2022 Oct 6;23(19):11877. doi: 10.3390/ijms231911877.

Abstract

Forkhead box O transcription factors (FoxOs) play an important role in maintaining normal cell physiology by regulating survival, apoptosis, autophagy, oxidative stress, the development and maturation of T and B lymphocytes, and the secretion of inflammatory cytokines. Cell types whose functions are regulated by FoxOs include keratinocytes, mucosal dermis, neutrophils, macrophages, dendritic cells, tumor-infiltrating activated regulatory T (Tregs) cells, B cells, and natural killer (NK) cells. FoxOs plays a crucial role in physiological and pathological immune responses. FoxOs control the development and function of Foxp3+ Tregs. Treg cells and Th17 cells are subsets of CD4+ T cells, which play an essential role in immune homeostasis and infection. Dysregulation of the Th17/Treg cell balance has been implicated in the development and progression of several disorders, such as autoimmune diseases, inflammatory diseases, and cancer. In addition, FoxOs are stimulated by the mitogen-activated protein (MAP) kinase pathway and inhibited by the PI3 kinase/AKT pathway. Downstream target genes of FoxOs include pro-inflammatory signaling molecules (toll-like receptor (TLR) 2, TLR4, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α), chemokine receptors (CCR7 and CXCR2), B-cell regulators (APRIL and BLYS), T-regulatory modulators (Foxp3 and CTLA-4), and DNA repair enzymes (GADD45α). Here, we review the recent progress in our understanding of FoxOs as the key molecules involved in immune cell differentiation and its role in the initiation of autoimmune diseases caused by dysregulation of immune cell balance. Additionally, in various diseases, FoxOs act as a cancer repressor, and reviving the activity of FoxOs forces Tregs to egress from various tissues. However, FoxOs regulate the cytotoxicity of both CD8+ T and NK cells against tumor cells, aiding in the restoration of redox and inflammatory homeostasis, repair of the damaged tissue, and activation of immune cells. A better understanding of FoxOs regulation may help develop novel potential therapeutics for treating immune/oxidative stress-related diseases.

摘要

叉头框 O 转录因子(FoxOs)通过调节细胞存活、细胞凋亡、自噬、氧化应激、T 和 B 淋巴细胞的发育和成熟以及炎症细胞因子的分泌,在维持正常细胞生理中发挥重要作用。FoxOs 调节功能的细胞类型包括角质形成细胞、黏膜真皮、中性粒细胞、巨噬细胞、树突状细胞、肿瘤浸润激活调节性 T(Treg)细胞、B 细胞和自然杀伤(NK)细胞。FoxOs 在生理和病理免疫反应中发挥着关键作用。FoxOs 控制 Foxp3+Treg 的发育和功能。Treg 细胞和 Th17 细胞是 CD4+T 细胞的亚群,在免疫稳态和感染中发挥着重要作用。Th17/Treg 细胞平衡的失调与自身免疫性疾病、炎症性疾病和癌症等多种疾病的发生和进展有关。此外,FoxOs 受丝裂原激活蛋白(MAP)激酶途径的刺激,受 PI3 激酶/AKT 途径的抑制。FoxOs 的下游靶基因包括促炎信号分子(Toll 样受体(TLR)2、TLR4、白细胞介素(IL)-1β和肿瘤坏死因子(TNF)-α)、趋化因子受体(CCR7 和 CXCR2)、B 细胞调节剂(APRIL 和 BLYS)、T 调节调节剂(Foxp3 和 CTLA-4)和 DNA 修复酶(GADD45α)。在这里,我们综述了 FoxOs 作为参与免疫细胞分化的关键分子的最新进展,以及其在免疫细胞平衡失调引起的自身免疫性疾病发生中的作用。此外,在各种疾病中,FoxOs 作为一种癌症抑制剂发挥作用,恢复 FoxOs 的活性迫使 Treg 从各种组织中迁出。然而,FoxOs 调节 CD8+T 细胞和 NK 细胞对肿瘤细胞的细胞毒性,有助于恢复氧化还原和炎症稳态、修复受损组织和激活免疫细胞。更好地了解 FoxOs 的调节作用可能有助于开发治疗免疫/氧化应激相关疾病的新潜在疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcf9/9569616/1b029d5bd8dd/ijms-23-11877-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验