该课题组定义了这种选择性主题小鼠的基础，其中Treg细胞对单个前列腺特异性自肽的反应被选择性地耗尽。该课题组人员发现，自我肽特异性Treg细胞在稳态下对匹配特异性的Tconv细胞的控制是必不可少的。
然而，它们需要控制这种Tconv细胞，并防止感染期间暴露于升高的自我肽后对前列腺产生自身免疫。重要的是，Treg细胞对自身肽的反应并不影响保护性Tconv细胞对病原体来源肽的反应。它们，自我肽特异性Treg细胞通过选择性控制共享自我特异性的Tconv细胞，在感染过程中促进自我非自我歧视。
据悉，在感染期间，CD4+ Foxp3+调节性T （Treg）细胞会控制自身反应性CD4+常规T （Tconv）细胞对自身肽抗原的反应，同时允许对病原体衍生的“非自身”肽的反应。
附：英文原文
Title: Regulatory T cells constrain T cells of shared specificity to enforce tolerance during infection
Author: David E. J. Klawon, Nicole Pagane, Matthew T. Walker, Nicole K. Ganci, Christine H. Miller, Eric Gai, Donald M. Rodriguez, Bridgett K. Ryan-Payseur, Ryan K. Duncombe, Erin J. Adams, Mark Maienschein-Cline, Nancy E. Freitag, Ronald N. Germain, Harikesh S. Wong, Peter A. Savage
Issue&Volume: 2025-02-27
Abstract: During infections, CD4+ Foxp3+ regulatory T (Treg) cells must control autoreactive CD4+ conventional T (Tconv) cell responses against self-peptide antigens while permitting those against pathogen-derived “nonself” peptides. We defined the basis of this selectivity using mice in which Treg cells reactive to a single prostate-specific self-peptide were selectively depleted. We found that self-peptide-specific Treg cells were dispensable for the control of Tconv cells of matched specificity at homeostasis. However, they were required to control such Tconv cells and prevent autoimmunity toward the prostate following exposure to elevated self-peptide during infection. Importantly, the Treg cell response to self-peptide did not impact protective Tconv cell responses to a pathogen-derived peptide. Thus, self-peptide-specific Treg cells promoted self-nonself discrimination during infection by selectively controlling Tconv cells of shared self-specificity.
DOI: adk3248
Source: https://www.science.org/doi/10.1126/science.adk3248