Interactions of the Immune System with Skin and Bone Tissue in Psoriatic Arthritis: A Comprehensive Review

Sukhov, Andrea; Adamopoulos, Iannis E.; Maverakis, Emanual

doi:10.1007/s12016-016-8529-8

Cited by 36 publications

(29 citation statements)

References 121 publications

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“…As presented below, TNIP1 is an oft-cited gene in GWAS studies with SNPs in certain populations suffering from systemic lupus erythematosus, psoriasis, and systemic sclerosis [ 13 – 16 ]. For recent consideration of possible genetic association of TNIP1 with other autoimmune diseases such as Sjögren syndrome and psoriatic arthritis, the reader is directed to [ 82 , 83 ].…”

Section: Tnip1 In Inflammation and Diseasementioning

confidence: 99%

TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling

Shamilov

Aneskievich

2018

Journal of Immunology Research

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TNIP1 protein is increasingly being recognized as a key repressor of inflammatory signaling and a potential factor in multiple autoimmune diseases. In addition to earlier foundational reports of TNIP1 SNPs in human autoimmune diseases and TNIP1 protein-protein interaction with receptor regulating proteins, more recent studies have identified new potential interaction partners and signaling pathways likely modulated by TNIP1. Subdomains within the TNIP1 protein as well as how they interact with ubiquitin have not only been mapped but inflammatory cell- and tissue-specific consequences subsequent to their defective function are being recognized and related to human disease states such as lupus, scleroderma, and psoriasis. In this review, we emphasize receptor signaling complexes and regulation of cytoplasmic signaling steps downstream of TLR given their association with some of the same autoimmune diseases where TNIP1 has been implicated. TNIP1 dysfunction or deficiency may predispose healthy cells to the inflammatory response to otherwise innocuous TLR ligand exposure. The recognition of the anti-inflammatory roles of TNIP1 and improved integrated understanding of its physical and functional association with other signaling pathway proteins may position TNIP1 as a candidate target for the design and/or testing of next-generation anti-inflammatory therapeutics.

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Section: Tnip1 In Inflammation and Diseasementioning

confidence: 99%

TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling

Shamilov

Aneskievich

2018

Journal of Immunology Research

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“…[48] The pathogenesis of PsA is not fully understood; however, findings from several studies suggest that IL-17 plays a role in disease development and progression, including genomewide association studies showing a link to IL-23/Th17 mediators such as IL-12B and IL-23R. [49] Using flow cytometry and Western blot analyses, Raychaudhuri and colleagues found that PsA-isolated synoviocytes have higher IL-17A receptor (IL-17RA) [50] levels than synoviocytes from patients with osteoarthritis and that the synovial fluid of patients with PsA has significantly higher levels of Th17 cells that produce functionally active IL-17 and that, in turn, induces upregulation of IL-6, IL-8 and MMP-3. Furthermore, in animal models of collageninduced arthritis, disruption of IL-17 signalling (IL-17-deficient mice and an anti-IL-17 antibody) protects against bone resorption.…”

Section: Psoriatic Arthritismentioning

confidence: 99%

Interleukin‐17 alters the biology of many cell types involved in the genesis of psoriasis, systemic inflammation and associated comorbidities

Krueger

Brunner

2017

Experimental Dermatology

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Psoriasis is a chronic, immune-mediated, systemic inflammatory disease that is defined by a characteristic skin reaction produced when elevated levels of inflammatory cytokines such as interleukin (IL)-17 alter the growth and differentiation of skin cells.The pathogenesis of comorbid conditions associated with psoriasis, including psoriatic arthritis, cardiovascular disease, obesity, metabolic syndrome, liver disorders, renal disease and depression, is also largely affected by inflammation. In this review, we examine the effect of IL-17 on the inflammatory pathways in a variety of different cell types, including keratinocytes, as well as epithelial cells of the colon, kidney, gut and liver. Additionally, we investigate the role of IL-17 in mediating the psoriasis-associated comorbidities detailed above. K E Y W O R D Scardiovascular disease, keratinocyte, metabolic syndrome, obesity, review

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“…The IL-23/IL-17 axis is also involved in the pathogenicity of PsA [ 46 ]. In addition to AS, polymorphisms in IL23R are a risk factor for PsA [ 47 ].…”

Section: Il-23 and Inflammatory Arthritismentioning

confidence: 99%

IL-23 and Th17 Disease in Inflammatory Arthritis

Yago

Nanke

Kawamoto

et al. 2017

JCM

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IL-23, which is composed of p19 and p40 subunits, is a proinflammatory cytokine that contributes to the formation and maintenance of Th17 cells in inflammatory autoimmune diseases. IL-23 is a human osteoclastogenic cytokine and anti-IL-23 antibody attenuates paw volume and joint destruction in CIA rats. IL-23 levels in serum and synovial fluid are high in rheumatoid arthritis (RA) patients, and IL-23 may be a useful biomarker for the diagnosis of RA. In addition, IL-23 affects the pathogenesis of inflammation and bone destruction through interaction with other cytokines such as IL-17 and TNF-α. Furthermore, polymorphisms of IL23R are a risk factor for ankylosing spondylitis (AS) and psoriatic arthritis (PsA), which indicates that IL-23 is also involved in the pathogenesis of spondyloarthritis (SpA). Finally, IL-17 and IL-23 inhibitors reduce the clinical manifestations of SpA. Thus, the IL-23/Th17 pathway is a therapeutic target for the treatment of inflammatory arthritis.

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Interactions of the Immune System with Skin and Bone Tissue in Psoriatic Arthritis: A Comprehensive Review

Cited by 36 publications

References 121 publications

TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling

TNIP1 in Autoimmune Diseases: Regulation of Toll-like Receptor Signaling

Interleukin‐17 alters the biology of many cell types involved in the genesis of psoriasis, systemic inflammation and associated comorbidities

IL-23 and Th17 Disease in Inflammatory Arthritis

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