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TL1A and allergic disease

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https://www.readbyqxmd.com/read/27896636/tnf-superfamily-cytokines-in-the-promotion-of-th9-differentiation-and-immunopathology
#1
REVIEW
Françoise Meylan, Richard M Siegel
The tumor necrosis factor (TNF) receptors and their corresponding cytokine ligands have been implicated in many aspects of the biology of immune functions. TNF receptors have key roles during various stages of T cell homeostasis. Many of them can co-stimulate lymphocyte proliferation and cytokine production. Additionally, several TNF cytokines can regulate T cell differentiation, including promoting Th1, Th2, Th17, and more recently the newly described Th9 subset. Four TNF family cytokines have been identified as regulators for IL-9 production by T cells...
November 28, 2016: Seminars in Immunopathology
https://www.readbyqxmd.com/read/26746844/insights-into-group-2-innate-lymphoid-cells-in-human-airway-disease
#2
REVIEW
Maya R Karta, David H Broide, Taylor A Doherty
Recent discoveries have led to the identification of a novel group of immune cells, the innate lymphoid cells (ILCs). The members of this group are divided into three subpopulations: ILC1s, ILC2s, and ILC3s. ILC2s produce Th2 cytokines, IL-4, IL-5, and IL-13, upon activation by epithelial cell-derived cytokines, lipid mediators (cysteinyl leukotrienes and prostaglandin D2), and TNF family member TL1A and promote structural and immune cell responses in the airways after antigen exposure. In addition, ILC2 function is also influenced by inducible T cell costimulator (ICOS)/ICOS-ligand (ICOS-L) interactions via direct contact between immune cells...
January 2016: Current Allergy and Asthma Reports
https://www.readbyqxmd.com/read/26188076/the-tnf-family-cytokine-tl1a-from-lymphocyte-costimulator-to-disease-co-conspirator
#3
REVIEW
Arianne C Richard, John R Ferdinand, Françoise Meylan, Erika T Hayes, Odile Gabay, Richard M Siegel
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...
September 2015: Journal of Leukocyte Biology
https://www.readbyqxmd.com/read/25786692/the-tnf-family-ligand-tl1a-and-its-receptor-dr3-promote-t-cell-mediated-allergic-immunopathology-by-enhancing-differentiation-and-pathogenicity-of-il-9-producing-t-cells
#4
Arianne C Richard, Cuiyan Tan, Eric T Hawley, Julio Gomez-Rodriguez, Ritobrata Goswami, Xiang-Ping Yang, Anthony C Cruz, Pallavi Penumetcha, Erika T Hayes, Martin Pelletier, Odile Gabay, Matthew Walsh, John R Ferdinand, Andrea Keane-Myers, Yongwon Choi, John J O'Shea, Aymen Al-Shamkhani, Mark H Kaplan, Igal Gery, Richard M Siegel, Françoise Meylan
The TNF family cytokine TL1A (Tnfsf15) costimulates T cells and type 2 innate lymphocytes (ILC2) through its receptor DR3 (Tnfrsf25). DR3-deficient mice have reduced T cell accumulation at the site of inflammation and reduced ILC2-dependent immune responses in a number of models of autoimmune and allergic diseases. In allergic lung disease models, immunopathology and local Th2 and ILC2 accumulation is reduced in DR3-deficient mice despite normal systemic priming of Th2 responses and generation of T cells secreting IL-13 and IL-4, prompting the question of whether TL1A promotes the development of other T cell subsets that secrete cytokines to drive allergic disease...
April 15, 2015: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/24368564/the-tnf-family-cytokine-tl1a-promotes-allergic-immunopathology-through-group-2-innate-lymphoid-cells
#5
F Meylan, E T Hawley, L Barron, J L Barlow, P Penumetcha, M Pelletier, G Sciumè, A C Richard, E T Hayes, J Gomez-Rodriguez, X Chen, W E Paul, T A Wynn, A N J McKenzie, R M Siegel
The tumor necrosis factor (TNF)-family cytokine TL1A (TNFSF15) costimulates T cells and promotes diverse T cell-dependent models of autoimmune disease through its receptor DR3. TL1A polymorphisms also confer susceptibility to inflammatory bowel disease. Here, we find that allergic pathology driven by constitutive TL1A expression depends on interleukin-13 (IL-13), but not on T, NKT, mast cells, or commensal intestinal flora. Group 2 innate lymphoid cells (ILC2) express surface DR3 and produce IL-13 and other type 2 cytokines in response to TL1A...
July 2014: Mucosal Immunology
https://www.readbyqxmd.com/read/22017439/tl1a-and-dr3-a-tnf-family-ligand-receptor-pair-that-promotes-lymphocyte-costimulation-mucosal-hyperplasia-and-autoimmune-inflammation
#6
REVIEW
Françoise Meylan, Arianne C Richard, Richard M Siegel
DR3 (TNFRSF25) is a member of the tumor necrosis factor receptor (TNFR) superfamily expressed primarily on lymphocytes and is a receptor for the TNF family cytokine TL1A (TNFSF15). DR3 costimulates T-cell activation, but it is unique among these receptors in that it signals through an intracytoplasmic death domain and the adapter protein TRADD (TNFR-associated death domain). TL1A costimulates T cells to produce a wide variety of cytokines and can promote expansion of activated and regulatory T cells in vivo...
November 2011: Immunological Reviews
https://www.readbyqxmd.com/read/18571443/the-tnf-family-receptor-dr3-is-essential-for-diverse-t-cell-mediated-inflammatory-diseases
#7
Françoise Meylan, Todd S Davidson, Erin Kahle, Michelle Kinder, Krishika Acharya, Dragana Jankovic, Virgilio Bundoc, Marcus Hodges, Ethan M Shevach, Andrea Keane-Myers, Eddie C Y Wang, Richard M Siegel
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...
July 18, 2008: Immunity
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