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T Cells Going Innate.

Authors: Midas Seyda|||Abdallah Elkhal|||Markus Quante|||Christine S Falk|||Stefan G Tullius

Journal: Trends in immunology

Publication Type: Journal Article

Date: 2016

DOI: NIHMS801918

ID: 27402226

Affiliations:

Affiliations

    Division of Transplant Surgery and Transplant Surgery Research Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Institute of Transplant Immunology, IFB-Tx, Hannover Medical School, Hannover, Germany.|||Division of Transplant Surgery and Transplant Surgery Research Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.|||Division of Transplant Surgery and Transplant Surgery Research Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.|||Institute of Transplant Immunology, IFB-Tx, Hannover Medical School, Hannover, Germany; German Center for Infection Research (DZIF), Hannover, Germany.|||Division of Transplant Surgery and Transplant Surgery Research Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: stullius@partners.org.

Abstract

Natural killer (NK) cell receptors (NKRs) play a crucial role in the homeostasis of antigen-experienced T cells. Indeed, prolonged antigen stimulation may induce changes in the receptor repertoire of T cells to a profile that features NKRs. Chronic antigen exposure, at the same time, has been shown to trigger the loss of costimulatory CD28 molecules with recently reported intensified antigen thresholds of antigen-experienced CD8(+) T cells. In transplantation, NKRs have been shown to assist allograft rejection in a CD28-independent fashion. We discuss here a role for CD28-negative T cells that have acquired the competency of the NKR machinery, potentially promoting allorecognition either through T cell receptor (TCR) crossreactivity or independently from TCR recognition. Collectively, NKRs can bring about innate-like T cells by providing alternative costimulatory pathways that gain relevance in chronic inflammation, potentially leading to resistance to CD28-targeting immunosuppressants.


Chemical List

    Antigens|||CD28 Antigens|||Receptors, Antigen, T-Cell|||Receptors, Natural Killer Cell

Reference List

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