Interleukin-7 enhances the Th1 response to promote the development of Sjögren's syndrome-like autoimmune exocrinopathy in mice - Wikidata - awgldk - TriplyDB

Interleukin-7 enhances the Th1 response to promote the development of Sjögren's syndrome-like autoimmune exocrinopathy in mice

Interleukin-7 enhances the Th1 response to promote the development of Sjögren's syndrome-like autoimmune exocrinopathy in mice

http://www.wikidata.org/entity/Q37060371

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The clinical relevance of animal models in Sjögren's syndrome: the interferon signature from mouse to man Innate immune signaling induces interleukin-7 production from salivary gland cells and accelerates the development of primary Sjögren's syndrome in a mouse model The important role of T cells and receptor expression in Sjögren's syndrome.Mouse Models of Primary Sjogren's Syndrome.Interleukin-7 produced by intestinal epithelial cells in response to Citrobacter rodentium infection plays a major role in innate immunity against this pathogen.Interleukin-6 inhibits apoptosis of exocrine gland tissues under inflammatory conditions Innate Immune Signaling Induces IL-7 Production, Early Inflammatory Responses, and Sjögren's-Like Dacryoadenitis in C57BL/6 Mice.Ginseng Berry Extract Attenuates Dextran Sodium Sulfate-Induced Acute and Chronic Colitis.A gene network regulated by the transcription factor VGLL3 as a promoter of sex-biased autoimmune diseases.Dendritic cells, T-cells and epithelial cells: a crucial interplay in immunopathology of primary Sjögren's syndrome.Update on Pathogenesis of Sjögren's syndrome.Prostatic acid phosphatase is the main acid phosphatase with 5'-ectonucleotidase activity in the male mouse saliva and regulates salivation.The Pathophysiology of Dry Eye Disease: What We Know and Future Directions for Research.Sjögren-Like Lacrimal Keratoconjunctivitis in Germ-Free Mice.Increased CCL25 and T Helper Cells Expressing CCR9 in the Salivary Glands of Patients With Primary Sjögren's Syndrome: Potential New Axis in Lymphoid Neogenesis.Editorial: interleukin-7 and its receptor: the axis of evil to target in Sjögren's syndrome?High salivary soluble L-selectin and interleukin-7 levels in Asian Indian patients with primary Sjögren's syndrome.Anti-IL-7 receptor-α treatment ameliorates newly established Sjögren's-like exocrinopathy in non-obese diabetic mice.Sjögren syndrome IL-7 receptor blockade blunts antigen-specific memory T cell responses and chronic inflammation in primates

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Interleukin-7 enhances the Th1 response to promote the development of Sjögren's syndrome-like autoimmune exocrinopathy in mice

http://www.wikidata.org/entity/Q37060371

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

@tr

scientific article published on August 2013

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Interleukin-7 enhances the Th1 ...... toimmune exocrinopathy in mice

@en

Interleukin-7 enhances the Th1 ...... oimmune exocrinopathy in mice.

@nl

type

label

Interleukin-7 enhances the Th1 ...... toimmune exocrinopathy in mice

@en

Interleukin-7 enhances the Th1 ...... oimmune exocrinopathy in mice.

@nl

prefLabel

Interleukin-7 enhances the Th1 ...... toimmune exocrinopathy in mice

@en

Interleukin-7 enhances the Th1 ...... oimmune exocrinopathy in mice.

@nl

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Arthritis & Rheumatology

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Interleukin-7 enhances the Th1 ...... toimmune exocrinopathy in mice

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Jun-O Jin

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Qing Yu

http://www.w3.org/2001/XMLSchema#string

Seunghee Cha

http://www.w3.org/2001/XMLSchema#string

Toshihisa Kawai

http://www.w3.org/2001/XMLSchema#string

P2860

Hepatic interleukin-7 expression regulates T cell responses

Proinflammatory cytokines tumor necrosis factor-alpha and interferon-gamma alter tight junction structure and function in the rat parotid gland Par-C10 cell line

Novel animal models for Sjögren's syndrome: expression and transfer of salivary gland dysfunction from regulatory T cell-deficient mice

Activation of innate immunity accelerates sialoadenitis in a mouse model for Sjögren's syndrome-like disease.

X-linked Foxp3 (Scurfy) mutation dominantly inhibits submandibular gland development and inflammation respectively through adaptive and innate immune mechanisms.

Activation of innate immune responses through Toll-like receptor 3 causes a rapid loss of salivary gland function

Resolvin D1 prevents TNF-α-mediated disruption of salivary epithelial formation

Development of Sjogren's syndrome in nonobese diabetic-derived autoimmune-prone C57BL/6.NOD-Aec1Aec2 mice is dependent on complement component-3.

Systemic autoimmunity and lymphoproliferation are associated with excess IL-7 and inhibited by IL-7Rα blockade.

Modeling Sjögren's syndrome with Id3 conditional knockout mice

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2132-2142

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scholarly article

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10.1002/ART.38007

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8

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65

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2013-08-01T00:00:00Z

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23666710

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3729733

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