Impairment of T-Cell Activation in Head and Neck Cancer In Situ and In Vitro

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Abstract
THE IMMUNE response against neoplastic cells is mediated by humoral as well as cellular effector mechanisms, with T cell–mediated immunity representing an essential component of antitumor responses.1 Generation of effective antitumor T-cell responses involves at least 3 stages of coordinated cell-to-cell interactions.2 Thus, adhesion, ie, the ability of lymphocytes to bind to antigen-presenting cells (APC) or tumor targets, is the first and obligatory step in antigen presentation.3 This is antigen-independent adhesion, mainly mediated by intercellular adhesion molecule-1 (ICAM-1) (CD54) and lymphocyte function associated antigen-3 (LFA-3) (CD58), expressed on APC and their respective counterreceptors, LFA-1 and CD2, expressed on the surface of T lymphocytes.4 Next, T-cell receptor–mediated recognition of a tumor antigen by T lymphocytes in the context of MHC molecules expressed on the surface of APC takes place. Subsequent proliferation of T cells in response to this antigen requires costimulation,2 resulting in a signal that is delivered to the nucleus and initiates cell division. In the absence of such signaling, the antigen-MHC interactions lead to T-cell anergy or apoptosis.2

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