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- W1995051048 abstract "It has become increasingly appreciated that signals mediated by the lymphotoxin beta receptor (LTßR), a tumor necrosis factor (TNF) family receptor, mediate various outcomes in both the developing and adult immune systems. In the adult animal, the LTαβ pathway is indispensable for the maintenance of stromal cell networks in the secondary lymphoid tissues. Since these networks are key controlling elements for the positioning of immune cells such as lymphocytes, it was hypothesized that blocking LTßR signaling may be a novel approach for inhibiting pathogenic autoimmune responses. To this end, multiple autoimmune models have been tested in mice that are genetically deficient in LTαβ/LTßR molecules or tested in mice that are treated with LTαβ/LIGHT pathway blocking agents. These studies have revealed an impressive array of autoimmune diseases that are sensitive to LTαβ/LIGHT pathway inhibition, signifying that blockade of LTßR-mediated signals has exciting clinical potential. A common element to these disease models is the recruitment, activation and migration of autoimmune T-lymphocytes. The mechanism of how blocking signals mediated by the LTßR influences autoimmune T-cell responses remains elusive, in particular because LTßR signaling appears to be critical at diverse biological levels. This review will describe the consequences of blocking LTßR-mediated signaling on autoimmune disease models, as well as models of infectious disease and will explore how LTßR activation may regulate T-lymphocyte responses." @default.
- W1995051048 created "2016-06-24" @default.
- W1995051048 creator A5021147315 @default.
- W1995051048 date "2004-10-01" @default.
- W1995051048 modified "2023-09-23" @default.
- W1995051048 title "A role for the lymphotoxin/LIGHT pathway in T-cell mediated autoimmunity and infectious disease" @default.
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- W1995051048 doi "https://doi.org/10.1016/j.cair.2004.07.001" @default.