CTLA-4 Control over Foxp3+ Regulatory T Cell Function

By K. Wing, Yasush Onishi, P. Prieto-Martin, Tomoyuki Yamaguchi, M. Miyara, Z. Fehérvári, T. Nomura, Shimon Sakaguchi. Science, 2008

3,038 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/26fc5d1ae31c2be3a3346b580ffa409aea9cb5f9

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Citations in the corpus

Autosomal-dominant immune dysregulation syndrome in humans with CTLA4 mutations (2014, positive): “CTLA-4 is an essential effector component of T reg cells that is required for their suppressive function 14-18 .”
Fc-dependent depletion of tumor-infiltrating regulatory T cells co-defines the efficacy of anti–CTLA-4 therapy against melanoma (2013, background): “, 2001), the demonstration that CD4+Foxp3+ regulatory T cells (T reg cell) express high levels of CTLA-4 led to the suggestion that –CTLA-4 directly impacts the T reg cell compartment, either by mediating depletion, or by affecting their suppressive activity (Read et al., 2000, 2006; Takahashi et a”
The emerging role of CTLA4 as a cell-extrinsic regulator of T cell responses (2011, background): “The most likely explanation for these differences is variation in the assay condition”
Anti-PD-1/PD-L1 therapy of human cancer: past, present, and future. (2015, positive): “Mice with Tregselective ablation of CTLA-4 recapitulate the majority of autoimmune phenotypes observed in traditional KO mice, including tissue-infiltrating T cells and damage to normal tissues and organs (71).”
Mechanisms of foxp3+ T regulatory cell-mediated suppression. (2009, positive): “The function of CTLA-4 on Treg cells has been somewhat clarified by the recent demonstration that animals with a selective deletion of expression of CTLA-4 develop systemic autoimmunity at 7 weeks of age (Wing et al., 2008).”
CD28 and CTLA-4 coreceptor expression and signal transduction (2009, background): “Lastly, recent evidence indicates that CTLA-4 is needed for the optimal function of regulatory T cells (Tregs) (31).”
Treg cells expressing the co-inhibitory molecule TIGIT selectively inhibit pro-inflammatory Th1 and Th17 cell responses (2014, background): “Coinhibitory molecules such as CTLA-4 and PD-1 not only serve as markers for T cell acti- vation but also contribute to Treg cell stability and function (Francisco et al., 2009; Wing et al., 2008), indicating that TIGIT+ Treg cells might be better equipped for mediating suppression.”