2020
DOI: 10.1097/cm9.0000000000001228
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Autoantibodies in psoriatic arthritis: are they of pathogenic relevance?

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Cited by 3 publications
(3 citation statements)
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“…[31] The mechanism of Dkk-1 in bone destruction seems to be regulated by cytokines in the local inflammatory microenvironments of joints, such as TNF-a, interleukin (IL)-6, IL-8, IL-17, and matrix metalloproteinases. [22,25,32,33] The cytokines interacted within a complicated regulatory network in inflammatory arthritis, modulating the interactions among immune cells, fibroblast-like synoviocytes, and osteoblasts. Bone erosion and bone formation are successive processes in PsA, indicating that elevation of serum Dkk-1 is a predictive indicator for bone erosion.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…[31] The mechanism of Dkk-1 in bone destruction seems to be regulated by cytokines in the local inflammatory microenvironments of joints, such as TNF-a, interleukin (IL)-6, IL-8, IL-17, and matrix metalloproteinases. [22,25,32,33] The cytokines interacted within a complicated regulatory network in inflammatory arthritis, modulating the interactions among immune cells, fibroblast-like synoviocytes, and osteoblasts. Bone erosion and bone formation are successive processes in PsA, indicating that elevation of serum Dkk-1 is a predictive indicator for bone erosion.…”
Section: Discussionmentioning
confidence: 99%
“…Dkk-1 has also been observed to be associated with spondyloarthritis and even with erosive arthritis in patients with systemic lupus erythematosus [31] . The mechanism of Dkk-1 in bone destruction seems to be regulated by cytokines in the local inflammatory microenvironments of joints, such as TNF-α, interleukin (IL)-6, IL-8, IL-17, and matrix metalloproteinases [22,25,32,33] . The cytokines interacted within a complicated regulatory network in inflammatory arthritis, modulating the interactions among immune cells, fibroblast-like synoviocytes, and osteoblasts.…”
Section: Discussionmentioning
confidence: 99%
“…Consistent with an autoimmune inflammation in PsA is the recently reported clonal expansion of CD8 + T cells in the synovial fluid of PsA 11. Further, diverse autoantibodies have been reported in PsA, although their pathogenicity has not been established 12 13. In addition to HLA, non-HLA innate immunity genes have been associated with psoriasis and PsA, suggesting the pathogenic relevance of innate immune dysfunction 1.…”
Section: Introductionmentioning
confidence: 75%