Please use this identifier to cite or link to this item:
|Title:||Modulation of antigen-specific T-cells as immune therapy for chronic infectious diseases and cancer|
|Keywords:||Tolerance induction;Antigen-specific T cells;Bystander T-cells;NanoAPC;Reverse tolerance|
|Citation:||Frontiers in Immunology, 5: Article 293,(2014)|
|Abstract:||T-cell responses are induced by antigen presenting cells (APC) and signals from the microenvironment. Antigen persistence and inflammatory microenvironments in chronic infections and cancer can induce a tolerant state in T-cells resulting in hyporesponsiveness, loss of effector function, and weak biochemical signaling patterns in response to antigen stimulation. Although the mechanisms of T-cell tolerance induced in chronic infection and cancer may differ from those involved in tolerance to self-antigen, the impaired proliferation and production of IL-2 in response to antigen stimulation are hallmarks of all tolerant T cells. In this review, we will summarize the evidence that the immune responses change from non-self to “self”-like in chronic infection and cancer, and will provide an overview of strategies for re-balancing the immune response of antigen-specific T cells in chronic infection and cancer without affecting the homeostasis of the immune system.|
|Description:||Copyright: © 2014 Li, Symonds, Miao, Sanderson and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.|
This article has been made available through the Brunel Open Access Publishing Fund.
|Appears in Collections:||Biological Sciences|
Brunel OA Publishing Fund
Dept of Life Sciences Research Papers
Items in BURA are protected by copyright, with all rights reserved, unless otherwise indicated.