![]() ![]() ![]() These cytokine signals likely further cement the activation and differentiation of the responding T cells ( 10, 11). ICAM-1–LFA-1 interactions have also been proposed to enhance IL-2 production by CD8 T cells, particularly during the early stages of the response ( 6). As the responding cells swarm, LFA-1 and ICAM-1 expressed upon T cells mediates T-cell–T-cell interactions and facilitates the directional secretion of IL-2 from one responding cell to another ( 8, 9). Expression of ICAM-1 by the APCs also lowers the concentration of antigen required to activate a naïve T cell ( 5), thereby enhancing the strength of antigenic stimulation, and engagement of LFA-1 by ICAM-1 has been proposed to have a costimulatory role ( 6, 7). Interactions governed by ICAM-1 can influence T-cell differentiation by promoting long duration contacts with APCs ( 3) and by facilitating asymmetric cell division ( 4). All these events are influenced by interactions mediated by intercellular adhesion molecule-1 (ICAM-1), (CD54) and its primary ligand, lymphocyte function-associated antigen (LFA)-1. Among the early commands that T cells receive, the strength of antigenic stimulation, the duration of contact with antigen-presenting cells (APCs), and cytokine signals have been proposed to instruct their subsequent development ( 1, 2). This cellular intimacy, coupled with the detection of other triggers, shapes the fate decisions of the responding T cells. The initial priming of naïve CD8 T cells, and the subsequent activation of effector and memory T cells, critically depends upon their ability to interrogate and respond to the arrays of MHC class I molecules present on the surface of the target cell. Collectively, these studies reveal potential dual roles for ICAM-1 in both promoting the decay of effector responses and programming the sensitivity of memory CD8 T cells to secondary stimuli. Although memory T cells do emerge and are maintained if ICAM-1 expression is abolished, the secondary proliferative capacity of these T cells is severely curtailed. ![]() Nevertheless, ICAM-1 expression on nonlymphocytes dictates the phenotypic and functional attributes of the antiviral CD8 T-cell populations that develop and promotes the gradual attrition of residual effector-like CD127 lo, KLRG-1 hi CD8 T cells during the memory phase of the response. Here we show that, following a prototypic acute viral infection, the formation and maintenance of memory-phenotype CD127 hi, KLRG-1 lo CD8 T cells does not require ICAM-1. Although previous studies suggest that ICAM-1 is essential for establishing memory T-cell populations following peptide immunization, the roles of ICAM-1 in antiviral cellular immunity are less well understood. Intercellular adhesion molecule (ICAM)-1 functions to enhance the strength of antigenic stimulation, extend the duration of contact with antigen-presenting cells, and augment cytokine signals, which are all factors that influence peripheral CD8 T-cell differentiation. The induction and properties of these responses are governed by a series of integrated processes that rely heavily on cell–cell interactions. CD8 T-cell responses are critical for protection against intracellular pathogens and tumors. ![]()
0 Comments
Leave a Reply. |
Details
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |