Abstract:Secretion of the proinflammatory cytokine Interleukin-17A (IL-17A) is the hallmark of a unique lineage of CD4 T cells designated Th17 cells, which may play a crucial role in the pathogenesis of rheumatoid arthritis (RA) and many autoimmune diseases. Recently, IL-17-producing cells other than T cells have been described, including diverse innate immune cells. Here, we show that the cellular sources of IL-17A in RA include a significant number of non-T cells. Multicolour fluorescence analysis of IL-17-expressing… Show more
“…76 Evidence suggests that B cells contribute to RA pathology by producing autoantibodies that initiate the complement cascade and promote selective antigen uptake. 77 In addition, B cells also present antigen to T cells, provide co-stimulation, release inflammatory cytokines 78,79 and contribute to RA-associated osteoclast activation and bone destruction through expression of RANKL. 80,81 Lack of IL-10 + regulatory B (B REG ) cell activity, through low frequencies or defective function, has also been suggested to contribute to RA.…”
In addition to its well-documented involvement in mineral homeostasis, vitamin D seems to have broad effects on human health that go beyond the skeletal system. Prominent among these so-called nonclassical effects of vitamin D are its immunomodulatory properties. In vitro studies have shown anti-inflammatory effects of 1,25-dihydroxyvitamin D (1,25(OH)2D), the active form of vitamin D. In addition, epidemiological analysis of patients with established inflammatory disease identified associations between vitamin D deficiency (low serum concentrations of inactive 25-hydroxyvitamin D, abbreviated to 25(OH)D) and inflammatory conditions, including rheumatoid arthritis (RA). The association of vitamin D deficiency with RA severity supports the hypothesis of a role for vitamin D in the initiation or progression of the disease, or possibly both. However, whether 25(OH)D status is a cause or consequence of RA is still incompletely understood and requires further analysis in prospective vitamin D supplementation trials. The characterization of factors that promote the transition from preclinical to clinical phases of RA has become a major focus of research, with the aim to facilitate earlier diagnosis and treatment, and improve therapeutic outcomes. In this Review, we aim to describe the current knowledge of vitamin D and the immune system specifically in RA, and discuss the potential benefits that vitamin D might have on slowing RA progression.
“…76 Evidence suggests that B cells contribute to RA pathology by producing autoantibodies that initiate the complement cascade and promote selective antigen uptake. 77 In addition, B cells also present antigen to T cells, provide co-stimulation, release inflammatory cytokines 78,79 and contribute to RA-associated osteoclast activation and bone destruction through expression of RANKL. 80,81 Lack of IL-10 + regulatory B (B REG ) cell activity, through low frequencies or defective function, has also been suggested to contribute to RA.…”
In addition to its well-documented involvement in mineral homeostasis, vitamin D seems to have broad effects on human health that go beyond the skeletal system. Prominent among these so-called nonclassical effects of vitamin D are its immunomodulatory properties. In vitro studies have shown anti-inflammatory effects of 1,25-dihydroxyvitamin D (1,25(OH)2D), the active form of vitamin D. In addition, epidemiological analysis of patients with established inflammatory disease identified associations between vitamin D deficiency (low serum concentrations of inactive 25-hydroxyvitamin D, abbreviated to 25(OH)D) and inflammatory conditions, including rheumatoid arthritis (RA). The association of vitamin D deficiency with RA severity supports the hypothesis of a role for vitamin D in the initiation or progression of the disease, or possibly both. However, whether 25(OH)D status is a cause or consequence of RA is still incompletely understood and requires further analysis in prospective vitamin D supplementation trials. The characterization of factors that promote the transition from preclinical to clinical phases of RA has become a major focus of research, with the aim to facilitate earlier diagnosis and treatment, and improve therapeutic outcomes. In this Review, we aim to describe the current knowledge of vitamin D and the immune system specifically in RA, and discuss the potential benefits that vitamin D might have on slowing RA progression.
“…Thus our data of increased IL-17 production by NK cells of ERA patients may support this hypothesis since most of our patients were HLA B27 positive and had high KIR3DL1/2 expression. A study in RA has reported a large fraction of IL-17 producing non T cells as compared to controls, among these cells NK cells also formed a small proportion [28]. No data however is available on spondyloarthropathies.…”
“…1 This pro-inflammatory marker has been associated with the pathogenesis of several autoimmune diseases and human inflammatory conditions. 1 The current evidence suggests that IL-17A is involved in psoriasis, 7 rheumatoid arthritis, 8 multiple sclerosis, 9 inflammatory bowel diseases 10 and asthma. 11 Several studies have demonstrated the association between dietary factors and inflammatory markers.…”
Higher consumption of fruits and vegetables is inversely associated with serum hs-CRP but not IL-17 levels. Studies investigating the dietary patterns in association with IL-17 in other populations are recommended.
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