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Overview of Immune Tolerance Strategies
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Charles J. Hackett, Helen Quill
In some cases, the inflammatory responses initiated by the innate immune system may contribute to the activation of autoreactive cells. For example, bacterial infection of dendritic cells leads to B7 upregulation, enabling costimulatory signaling of T cells that may interact with any antigen presented by that particular dendritic cell. Cellular necrosis, occurring as a result of infection or tissue damage, as opposed to the self-destruction process of apoptosis, can trigger immature dendritic cells to become highly activated and to function as APC for T cells.9 Thus, self-antigens that happen to be presented in the context of B7 may activate autoimmune T cell responses. Note that several conditions must be present to initiate autoimmunity: the presentation of a sufficient amount of self antigen/MHC complexes by activated APC, availability of sufficiently high affinity autoreactive T cells in contact with the APC, and the unavailability or ineffectiveness of overriding regulatory cell activity.
Modelling combined virotherapy and immunotherapy: strengthening the antitumour immune response mediated by IL-12 and GM-CSF expression
Published in Letters in Biomathematics, 2018
Adrianne L. Jenner, Chae-Ok Yun, Arum Yoon, Adelle C. F. Coster, Peter S. Kim
Controlling the CTL induced apoptosis rates k could be achieved through the introduction of an experimental cancer treatment known as CTLA-4 blockades (Henson, Macaulay, Kiani-Alikhan, & Akbar, 2008; Parry et al., 2005). CTLA-4 is a well-known T cell inhibitory B7-receptor that is expressed by activated T cells. Using the CTLA-4 blockade, researchers have shown that this treatment can enhance T cell cytotoxic responses and induce the differentiation of cytotoxic CD4 T cells Leach et al. (1996). Therefore, one possible way to investigate whether perturbations in the CTL induced apoptosis rates k would result in the outcomes presented in Figure 3(e), would be to look at combining CTLA-4 blockades with oncolytic virus expressing IL-12 and GM-CSF.