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Kesley Attridge

Researcher at University of Birmingham

Publications -  12
Citations -  1917

Kesley Attridge is an academic researcher from University of Birmingham. The author has contributed to research in topics: T cell & IL-2 receptor. The author has an hindex of 8, co-authored 12 publications receiving 1598 citations. Previous affiliations of Kesley Attridge include Aston University & University of Oxford.

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Trans-Endocytosis of CD80 and CD86: A Molecular Basis for the Cell-Extrinsic Function of CTLA-4

TL;DR: A mechanism of immune regulation in which CTLA-4 acts as an effector molecule to inhibit CD28 costimulation by the cell-extrinsic depletion of ligands is revealed, accounting for many of the known features of the CD28–CTLA- 4 system.
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Follicular helper T cell signature in type 1 diabetes

TL;DR: A Tfh cell signature in autoimmune diabetes is identified and it is suggested that this population of islet-specific T cells could be used as a biomarker and potentially targeted for T1D interventions.
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IL-21 inhibits T cell IL-2 production and impairs Treg homeostasis

TL;DR: It is demonstrated that IL-21 and IL-2 can have overlapping roles in promoting conventional T-cell responses but play distinct roles in controlling Treg homeostasis and function, and this data suggest a new paradigm whereby cytokines can promote immunity by inhibitingIL-2.
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Cutting edge: cell-extrinsic immune regulation by CTLA-4 expressed on conventional T cells.

TL;DR: It is shown that Tconv-expressed CTLA-4 can function in a cell-extrinsic manner in vivo, and this observation provides a potential resolution to the above paradox and suggests CTla-4 function on both Tconv and regulatory T cells can be achieved through cell- Extrinsics mechanisms.
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Homeostasis and function of regulatory T cells (Tregs) in vivo: lessons from TCR-transgenic Tregs.

TL;DR: The identification of CD25 and subsequently Forkhead box protein 3 (Foxp3) as markers for regulatory T cells (Tregs) has revolutionized the ability to explore this population experimentally and yielded insights into genes required for Treg function in vivo, with particular progress being made on the role of ctla‐4.