Meylan, Françoise, Davidson, Todd S., Kahle, Erin, Kinder, Michelle, Acharya, Krishika, Jankovic, Dragana, Bundoc, Virgilio, Hodges, Marcus, Shevach, Ethan M., Keane-Myers, Andrea, Wang, Edward Chung Yern ORCID: https://orcid.org/0000-0002-2243-4964 and Siegel, Richard M. 2008. The TNF-family receptor DR3 is essential for diverse T cell-mediated inflammatory diseases. Immunity 29 (1) , pp. 79-89. 10.1016/j.immuni.2008.04.021 |
Abstract
DR3 (TRAMP, LARD, WSL-1, TNFRSF25) is a death-domain-containing tumor necrosis factor (TNF)-family receptor primarily expressed on T cells. TL1A, the TNF-family ligand for DR3, can costimulate T cells, but the physiological function of TL1A-DR3 interactions in immune responses is not known. Using DR3-deficient mice, we identified DR3 as the receptor responsible for TL1A-induced T cell costimulation and dendritic cells as the likely source for TL1A during T cell activation. Despite its role in costimulation, DR3 was not required for in vivo T cell priming, for polarization into T helper 1 (Th1), Th2, or Th17 effector cell subtypes, or for effective control of infection with Toxoplasma gondii. Instead, DR3 expression was required on T cells for immunopathology, local T cell accumulation, and cytokine production in Experimental Autoimmune Encephalomyelitis (EAE) and allergic lung inflammation, disease models that depend on distinct effector T cell subsets. DR3 could be an attractive therapeutic target for T cell-mediated autoimmune and allergic diseases.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Medicine Systems Immunity Research Institute (SIURI) |
Subjects: | Q Science > QR Microbiology > QR180 Immunology R Medicine > R Medicine (General) |
Uncontrolled Keywords: | molimmuno |
Publisher: | Elsevier |
ISSN: | 1074-7613 |
Last Modified: | 19 Oct 2022 10:47 |
URI: | https://orca.cardiff.ac.uk/id/eprint/25543 |
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