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Spreading spondyloarthritis: are ILCs cytokine shuttles from base camp gut?

Spreading spondyloarthritis: are ILCs cytokine shuttles from base camp gut?

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Whodunit? The Contribution of Interleukin (IL)-17/IL-22-Producing γδ T Cells, αβ T Cells, and Innate Lymphoid Cells to the Pathogenesis of Spondyloarthritis.

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Spreading spondyloarthritis: are ILCs cytokine shuttles from base camp gut?

http://www.wikidata.org/entity/Q49124951

description

2015 nî lūn-bûn

@nan

2015年の論文

@ja

2015年学术文章

@wuu

2015年学术文章

@zh

2015年学术文章

@zh-cn

2015年学术文章

@zh-hans

2015年学术文章

@zh-my

2015年学术文章

@zh-sg

2015年學術文章

@yue

2015年學術文章

@zh-hant

name

Spreading spondyloarthritis: are ILCs cytokine shuttles from base camp gut?

@en

Spreading spondyloarthritis: are ILCs cytokine shuttles from base camp gut?

@nl

type

label

Spreading spondyloarthritis: are ILCs cytokine shuttles from base camp gut?

@en

Spreading spondyloarthritis: are ILCs cytokine shuttles from base camp gut?

@nl

prefLabel

Spreading spondyloarthritis: are ILCs cytokine shuttles from base camp gut?

@en

Spreading spondyloarthritis: are ILCs cytokine shuttles from base camp gut?

@nl

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ANNRHEUMDIS-2015-207735

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Annals of the Rheumatic Diseases

P1476

Spreading spondyloarthritis: are ILCs cytokine shuttles from base camp gut?

@en

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Barbara Neerinckx

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Dirk Elewaut

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

Rik J Lories

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P2860

Association scan of 14,500 nonsynonymous SNPs in four diseases identifies autoimmunity variants

Frequency and phenotype of peripheral blood Th17 cells in ankylosing spondylitis and rheumatoid arthritis

The anatomical basis for disease localisation in seronegative spondyloarthropathy at entheses and related sites.

CCR7-dependent trafficking of RORγ⁺ ILCs creates a unique microenvironment within mucosal draining lymph nodes.

Analysis of IL-17(+) cells in facet joints of patients with spondyloarthritis suggests that the innate immune pathway might be of greater relevance than the Th17-mediated adaptive immune response

Mesenchymal cell targeting by TNF as a common pathogenic principle in chronic inflammatory joint and intestinal diseases.

Evidence that autophagy, but not the unfolded protein response, regulates the expression of IL-23 in the gut of patients with ankylosing spondylitis and subclinical gut inflammation

The biology of innate lymphoid cells.

Ustekinumab for the treatment of patients with active ankylosing spondylitis: results of a 28-week, prospective, open-label, proof-of-concept study (TOPAS).

In situ analysis of interleukin-23- and interleukin-12-positive cells in the spine of patients with ankylosing spondylitis.

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1633-1635

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scholarly article

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10.1136/ANNRHEUMDIS-2015-207735

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9

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280392649

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26199396

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