The role of TNFRSF25:TNFSF15 in disease⋯ and health?

Taylor H. Schreiber, Dietlinde Wolf, Eckhard R. Podack

Research output: Chapter in Book/Report/Conference proceedingConference contribution

10 Scopus citations

Abstract

TNFRSF25 (DR3) is one of the most recently discovered TNF superfamily receptors and includes an intracellular death domain required to initiate signaling. Over the past decade significant progress has been made in defining the characteristics of this receptor, including the identification of its ligand, TNFSF15 (TL1A). Although TL1A can be provided from a number of sources, signaling through TNFRSF25 is primarily concentrated on T cells. TNFRSF25 signaling can lower the threshold for TCR-induced cell proliferation or cytokine production in an IL-2-dependent manner as well as amplify cytokine production initiated by IL-12 and IL-18. In vivo, TNFRSF25:TL1A signaling has been associated with a number of autoinflammatory conditions including allergic asthma, experimental autoimmune encephalomyelitis, type 1 diabetes, rheumatoid arthritis, and inflammatory bowel disease. Here we discuss the short history of TL1A:TNFRSF25 in health and disease states, including several exciting new observations reported at the 12th international TNF conference, 2009.

Original languageEnglish (US)
Title of host publicationAdvances in TNF Family Research
Subtitle of host publicationProceedings of the 12th International TNF Conference, 2009
EditorsDavid Wallach, Andrew Kovalenko, Marc Feldmann
Pages289-298
Number of pages10
DOIs
StatePublished - Dec 15 2011

Publication series

NameAdvances in Experimental Medicine and Biology
Volume691
ISSN (Print)0065-2598

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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    Schreiber, T. H., Wolf, D., & Podack, E. R. (2011). The role of TNFRSF25:TNFSF15 in disease⋯ and health? In D. Wallach, A. Kovalenko, & M. Feldmann (Eds.), Advances in TNF Family Research: Proceedings of the 12th International TNF Conference, 2009 (pp. 289-298). (Advances in Experimental Medicine and Biology; Vol. 691). https://doi.org/10.1007/978-1-4419-6612-4_30