T‐cell exhaustion: understanding the interface of chronic viral and autoinflammatory diseases. Issue 10 (1st November 2016)

• Record Type: Journal Article
• Authors: McKinney, Eoin F; Smith, Kenneth GC
• Is Part Of: Immunology and cell biology. Volume 94:Issue 10(2016)
• Page Start: 935
• Page End: 942
• Publication Date: 2016-11-01
• Subjects: Immunology -- Periodicals; Cytology -- Periodicals; 616.079
• DOI: 10.1038/icb.2016.81
• Languages: English
• ISSNs: 0818-9641

Abstract

Abstract : During acute viral infection CD8 T cells rapidly expand before contracting down to a persistent memory population that confers long‐lasting immunity. However when the antigen persists, such as during chronic viral infection, a dysfunctional process termed 'exhaustion' limits the antiviral response, facilitating ongoing viraemia and poor clinical outcome. CD8 T‐cell exhaustion was originally identified in lymphocytic choriomeningitis virus infection of mice; however, new evidence has shown that exhaustion is associated with the control of a wide range of human chronic inflammatory states, including chronic viral infection, autoimmunity and cancer. Consequently, an understanding of the mechanisms controlling exhaustion during chronic infection may also indicate new strategies for controlling other chronic inflammatory diseases. In particular, the success of immune checkpoint blockade as a form of cancer immunotherapy has prompted renewed efforts to understand how T‐cell immunity to chronic antigenic stimulation might similarly be measured or modulated in autoimmune diseases. Here we summarise the mechanisms controlling T‐cell exhaustion and how they relate to the control of autoimmune responses, providing a future perspective on measuring or manipulating exhaustion to personalise therapy. Abstract : The November/December 2016 issue contains a Special Feature on Novel aspects of autoimmunity. Major scientific advances often arise at the interface of disciplines, or are made possible by transformative technological advances. Progress in our understanding of the basis of autoimmunity over recent years provides great examples of this, and we have selected four of these to highlight in this ICB Special Feature. Together these articles reveal how recent technological advances have revealed important mechanisms underlying autoimmune disease, mechanisms that can now be examined in humans as well as mouse models. Our increasing ability to conduct in‐depth studies in humans promises to continue to unlock the mysteries underlying autoimmunity, with inevitable benefits to patients with these diseases. Immunology & Cell Biology thanks the coordinators of this Special Feature ‐ Ken Smith and Arthur Kaser ‐ for their planning and input.