FOXP3+免疫应答调节因子的发育和功能。
Development and Function of FOXP3 + Regulators of Immune Responses.
发表日期:2023 Apr 22
作者:
Mahdieh Golzari-Sorkheh, Juan Carlos Zúñiga-Pflücker
来源:
Cellular & Molecular Immunology
摘要:
Forkhead Box P3(FOXP3)蛋白质是调节性T细胞(Tregs)发育和功能的必要转录因子,参与免疫耐受的维持。虽然过去十年的广泛研究已经调查了FOXP3 +细胞在维持免疫稳态方面的关键作用,但我们对它们具体功能的了解仍然有限。因此,揭示FOXP3上游和下游转录调控的分子机制对于开发Treg靶向治疗至关重要。同时,发现FOXP3 + Tregs的功能失调也是自身免疫性疾病的内在驱动因素,并在癌症环境下展现出多方面的功能。最近的研究表明,这些细胞也可能参与特定组织的修复和再生。在本文中,我们总结了FOXP3 + Tregs的胸腺 - 转录调控景观、它们的表观遗传学调控因子以及相关的信号通路的现有认识。最后,我们重点强调了FOXP3对Tregs功能发展的贡献,并反思其在病理和生理免疫应答方面的临床意义。 ©作者 2023。本文发表于牛津大学出版社,代表英国免疫学会的立场。保留所有权利。请发送电子邮件至journals.permissions@oup.com以获取权限。
The Forkhead Box P3 (FOXP3) protein is an essential transcription factor for the development and function of regulatory T cells (Tregs), involved in the maintenance of immunological tolerance. Although extensive research over the last decade has investigated the critical role of FOXP3 + cells in preserving immune homeostasis, our understanding of their specific functions remains limited. Therefore, unveiling the molecular mechanisms underpinning the up- and downstream transcriptional regulation of and by FOXP3 is crucial for developing Treg-targeted therapeutics. Dysfunctions in FOXP3 + Tregs have also been found to be inherent drivers of autoimmune disorders, and have been shown to exhibit multifaceted functions in the context of cancer. Recent research suggests that these cells may also be involved in tissue-specific repair and regeneration. Herein, we summarize current understanding of the thymic-transcriptional regulatory landscape of FOXP3 + Tregs, their epigenetic modulators, and associated signaling pathways. Lastly, we highlight the contributions of FOXP3 on the functional development of Tregs, and reflect on the clinical implications in the context of pathological and physiological immune responses.© The Author(s) 2023. Published by Oxford University Press on behalf of the British Society for Immunology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.