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J Leukoc Biol. 2015 Sep;98(3):333-45. doi: 10.1189/jlb.3RI0315-095R. Epub 2015 Jul 17.

The TNF-family cytokine TL1A: from lymphocyte costimulator to disease co-conspirator.

Author information

1
*Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
2
*Immunoregulation Section, Autoimmunity Branch, NIAMS, National Institutes of Health, Bethesda, Maryland, USA; Cambridge Institute for Medical Research and Department of Medicine, University of Cambridge, Cambridge, United Kingdom; Cancer Sciences Academic Unit, Faculty of Medicine, University of Southampton, Southampton, United Kingdom rsiegel@nih.gov.

Abstract

Originally described in 2002 as a T cell-costimulatory cytokine, the tumor necrosis factor family member TNF-like factor 1A (TL1A), encoded by the TNFSF15 gene, has since been found to affect multiple cell lineages through its receptor, death receptor 3 (DR3, encoded by TNFRSF25) with distinct cell-type effects. Genetic deficiency or blockade of TL1A-DR3 has defined a number of disease states that depend on this cytokine-receptor pair, whereas excess TL1A leads to allergic gastrointestinal inflammation through stimulation of group 2 innate lymphoid cells. Noncoding variants in the TL1A locus are associated with susceptibility to inflammatory bowel disease and leprosy, predicting that the level of TL1A expression may influence host defense and the development of autoimmune and inflammatory diseases.

KEYWORDS:

DR3; autoimmune disease

PMID:
26188076
PMCID:
PMC4763597
DOI:
10.1189/jlb.3RI0315-095R
[Indexed for MEDLINE]
Free PMC Article

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