Th17 cells expressing KIR3DL2+ and responsive to HLA-B27 homodimers are increased in ankylosing spondylitis.
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HLA-B27 and psoriatic disease: a modern view of an old relationshipHLA-B27 misfolding and ankylosing spondylitisReview: The interleukin-23/interleukin-17 axis in spondyloarthritis pathogenesis: Th17 and beyondHLA-B27-Homodimer-Specific Antibody Modulates the Expansion of Pro-Inflammatory T-Cells in HLA-B27 Transgenic RatsHLA-F and MHC class I open conformers are ligands for NK cell Ig-like receptorsInteractions of the Immune System with Skin and Bone Tissue in Psoriatic Arthritis: A Comprehensive Review.Autoimmune epididymoorchitis is essential to the pathogenesis of male-specific spondylarthritis in HLA-B27-transgenic ratsERAP1 reduces accumulation of aberrant and disulfide-linked forms of HLA-B27 on the cell surfaceEndoplasmic reticulum aminopeptidase-1 alleles associated with increased risk of ankylosing spondylitis reduce HLA-B27 mediated presentation of multiple antigens.Two new cases of KIR3DP1, KIR2DL4-negative genotypes, one of which is also lacking KIR3DL2.Inhibiting HLA-B27 homodimer-driven immune cell inflammation in spondylarthritis.Update on ankylosing spondylitis: current concepts in pathogenesis.Functionally distinct ERAP1 allotype combinations distinguish individuals with Ankylosing Spondylitis.Interleukin 15 primes natural killer cells to kill via NKG2D and cPLA2 and this pathway is active in psoriatic arthritis.Targeted delivery of an antigenic peptide to the endoplasmic reticulum: application for development of a peptide therapy for ankylosing spondylitis.Role of IL-38 and its related cytokines in inflammationImmune cell transcript modules reveal leukocyte heterogeneity in synovial biopsies of seronegative spondylarthropathy patients.The danger model approach to the pathogenesis of the rheumatic diseases.Characterization of the recognition specificity of BH2, a monoclonal antibody prepared against the HLA-B27 heavy chain.IL-38 binds to the IL-36 receptor and has biological effects on immune cells similar to IL-36 receptor antagonistPemphigus is associated with KIR3DL2 expression levels and provides evidence that KIR3DL2 may bind HLA-A3 and A11 in vivo.CBP30, a selective CBP/p300 bromodomain inhibitor, suppresses human Th17 responsesAllele-Independent Turnover of Human Leukocyte Antigen (HLA) Class Ia MoleculesAnkylosing spondylitis patients display altered dendritic cell and T cell populations that implicate pathogenic roles for the IL-23 cytokine axis and intestinal inflammationSulfasalazine Treatment Suppresses the Formation of HLA-B27 Heavy Chain Homodimer in Patients with Ankylosing Spondylitis.IL-23/Th17 axis is not influenced by TNF-blocking agents in ankylosing spondylitis patientsSilencing or inhibition of endoplasmic reticulum aminopeptidase 1 (ERAP1) suppresses free heavy chain expression and Th17 responses in ankylosing spondylitis.Activation-Induced Killer Cell Immunoglobulin-like Receptor 3DL2 Binding to HLA-B27 Licenses Pathogenic T Cell Differentiation in Spondyloarthritis.Non-conventional forms of HLA-B27 are expressed in spondyloarthritis joints and gut tissue.Inflammation activation and resolution in human tendon disease.KIR3DL2 binds to HLA-B27 dimers and free H chains more strongly than other HLA class I and promotes the expansion of T cells in ankylosing spondylitisThe arthritis-associated HLA-B*27:05 allele forms more cell surface B27 dimer and free heavy chain ligands for KIR3DL2 than HLA-B*27:09.17 and 23: prime numbers for ankylosing spondylitis?HLA-B27 alters the response to tumor necrosis factor α and promotes osteoclastogenesis in bone marrow monocytes from HLA-B27-transgenic rats.Combined effects of ankylosing spondylitis-associated ERAP1 polymorphisms outside the catalytic and peptide-binding sites on the processing of natural HLA-B27 ligandsUpdate on juvenile spondyloarthritis.Role of HLA-B27 in the pathogenesis of ankylosing spondylitis (Review).Endoplasmic reticulum aminopeptidase 1 and interleukin-23 receptor in ankylosing spondylitis.Cells of the immune system orchestrate changes in bone cell function.Immune cells and bone: coupling goes both ways.
P2860
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P2860
Th17 cells expressing KIR3DL2+ and responsive to HLA-B27 homodimers are increased in ankylosing spondylitis.
description
2011 nî lūn-bûn
@nan
2011 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Th17 cells expressing KIR3DL2+ ...... sed in ankylosing spondylitis.
@ast
Th17 cells expressing KIR3DL2+ ...... sed in ankylosing spondylitis.
@en
type
label
Th17 cells expressing KIR3DL2+ ...... sed in ankylosing spondylitis.
@ast
Th17 cells expressing KIR3DL2+ ...... sed in ankylosing spondylitis.
@en
prefLabel
Th17 cells expressing KIR3DL2+ ...... sed in ankylosing spondylitis.
@ast
Th17 cells expressing KIR3DL2+ ...... sed in ankylosing spondylitis.
@en
P2093
P2860
P356
P1476
Th17 cells expressing KIR3DL2+ ...... sed in ankylosing spondylitis.
@en
P2093
Andrew McMichael
Anna Ridley
Antoni T Chan
Fraser Cummings
Isabel Wong-Baeza
Jacqueline Shaw
Myles Fleming
Paul Bowness
Simon Kollnberger
P2860
P304
P356
10.4049/JIMMUNOL.1002653
P407
P577
2011-01-19T00:00:00Z