Features of responding T cells in cancer and chronic infection.
Ever since T cell exhaustion was initially characterized and thoroughly analyzed in the murine LCMV model, such a functional impairment has been validated in other chronic viral infections such as HIV, HCV, and HBV. In tumor immunology, it has always been postulated that tumor-reactive T cells could also become functionally exhausted owing to the high tumor-antigen load and accompanying inhibitory mechanisms. However, the empirical evidences for this hypothesis have not been as extensive as in chronic infection perhaps because much of the focus on T cell dysfunction in tumor immunology has been, and appropriately so, on breaking or bypassing immune tolerance and anergy to tumor/self antigens. On the basis of recent reports, it is becoming clear that T cell exhaustion also plays a crucial role in the impairment of antitumor immunity. In this review, we will comparatively evaluate the T cell responses in cancer and chronic infection, and the therapeutic strategies and interventions for both diseases.
Kim
Peter S
PS
Emory Vaccine Center, Emory University School of Medicine, Atlanta, GA 30322, USA.
Ahmed
Rafi
R
D000818:Animals; D015703:Antigens, CD; D051017:Apoptosis Regulatory Proteins; D019496:Cancer Vaccines; D002908:Chronic Disease; D006801:Humans; D007111:Immunity, Cellular; D007165:Immunosuppression Therapy; D007167:Immunotherapy; D051379:Mice; D009369:Neoplasms / Q000276:immunology* / Q000628:therapy; D061026:Programmed Cell Death 1 Receptor; D013601:T-Lymphocytes / Q000276:immunology*; D014777:Virus Diseases / Q000276:immunology* / Q000628:therapy
D015703:Antigens, CD; D051017:Apoptosis Regulatory Proteins; D019496:Cancer Vaccines; C105992:PDCD1 protein, human; D061026:Programmed Cell Death 1 Receptor