In Situ Analysis of Interleukin–23– and Interleukin‐12–Positive Cells in the Spine of Patients With Ankylosing Spondylitis

Appel, Heiner; Maier, R.; Bleil, J.; Hempfing, Axel; Loddenkemper, Christoph; Schlichting, Uwe; Syrbe, Uta; Sieper, Joachim

doi:10.1002/art.37937

Cited by 130 publications

(88 citation statements)

References 35 publications

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“…Infection also stimulates the up-regulation of T cells to maintain immune homeostasis [4]. There are increasing findings suggesting the involvement of T cells in AS [5,6]. Recent studies reveal that disordered T cells are observed in peripheral blood and inflammatory joints from patients with AS [7,8].…”

Section: Introductionmentioning

confidence: 97%

MicroRNA let-7i induced autophagy to protect T cell from apoptosis by targeting IGF1R

Hou

Zhu

Sun

et al. 2014

Biochemical and Biophysical Research Communications

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Section: Introductionmentioning

confidence: 97%

MicroRNA let-7i induced autophagy to protect T cell from apoptosis by targeting IGF1R

Hou

Zhu

Sun

et al. 2014

Biochemical and Biophysical Research Communications

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“…Although IL-23 serum levels (14,(40)(41)(42) and IL-23 expression in the subchondral bone marrow from the facet joints (26) are up-regulated in AS patients, no correlation has been found with MRI inflammation or clinical DA (24). As IL-17 and IL-23 levels fall significantly in responders to anti-TNFα drugs and rise in non-responders (41), both cytokines (IL-17, IL-23) are considered promising therapeutic targets (42,43). In addition, IL-22 interconnected with IL-17 and Th17 cells is elevated in patients with AS (43).…”

Section: Original Papermentioning

confidence: 99%

“…As IL-17 and IL-23 levels fall significantly in responders to anti-TNFα drugs and rise in non-responders (41), both cytokines (IL-17, IL-23) are considered promising therapeutic targets (42,43). In addition, IL-22 interconnected with IL-17 and Th17 cells is elevated in patients with AS (43). When IL-17, IL-22 and IL-23 were examined in our patients, they were found to be below detection levels in all three patient cohorts.…”

Section: Original Papermentioning

confidence: 99%

Biomarkers, imaging and disease activity indices in patients with early axial spondyloarthritis: the Italian arm of the SpondyloArthritis-Caught-Early (SPACE) Study

Lorenzin¹,

Ortolan

Vio

et al. 2017

Reumatismo

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The study aimed to evaluate biomarkers facilitating early diagnosis of axial spondyloarthritis (axSpA) and correlations between them and disease activity parameters and imaging indexes. Patients with low back pain (LBP) (≥3 months, ≤2 years, onset ≤45 years) participating in the Italian arm of the SpondyloArthritis-Caught-Early SPACE study underwent a physical examination, questionnaires, laboratory tests, X-rays and MRI of the spine and sacroiliac joints (SIJ). An expert rheumatologist formulated axSpA diagnosis in accordance with Assessment of SpondyloArthritis International Society (ASAS) criteria. Disease activity and physical functioning were assessed using imaging, clinical and serological indices. Spine and SIJ MRI and X-rays were scored independently by 2 readers using the SPARCC, mSASSS and NY-criteria. Patients were classified as: subjects with signs of radiographic sacroiliitis (r-axSpA), subjects with signs of sacroiliitis on SIJ-MRI but not on X-rays (nr-axSpA MRI SIJ+) or subjects with no signs of sacroiliitis on MRI/X-rays but with >2 SpA features and signs of bone oedema on MRI spine (nr-axSpA MRI SIJ-/undifferentiated SpA). Significant differences were found in the prevalence of radiographic sacroiliitis, active sacroiliitis on MRI and SPARCC SIJ scores. Biomarker levels were not significantly increased in any of the patient groups. The correlations between IL-17 and IL-23 and other indices were not significant; correlations were found between IL-22 and BASFI, BASG1, HAQ, VAS pain, between mSASSS and MMP3, and between the latter and hsCRP. Although not significantly higher in any of the three groups, IL-22, MMP3 and hsCRP values were correlated with some disease activity indexes and with mSASSS. Large observational studies are required to confirm these preliminary findings.

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“…Synovial fluid in patients with SpA shows elevated concentration of IL-23 [23]. High expression of this cytokine has also been found in vertebral facet joints, where the cytokine is produced by macrophages residing in fibrous tissue and neutrophils, macrophages, and dendritic cells found in subchondral bone marrow [24].…”

Section: Cytokine Involvement In Arthritismentioning

confidence: 99%

New aspects of spondyloarthritis pathogenesis. Part III – arthritis, pathological bone remodeling

Kontny¹

2014

Reumatologia

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Słowa kluczowe: procesy destrukcyjne, patologiczna przebudowa kości, cytokiny. S t r e s z c z e n i eSpondyloartropatie (SpA) są formą przetrwałego zapalenia stawów obwodowych i kręgosłupa, które może być zapoczątkowane przez zapalenie podchrzęstnego szpiku kostnego w stawach albo zapalenie przyczepów ścięgnistych. Inwazyjna tkanka włóknista zastępu-jąca szpik kostny, rezydujące w przyczepach ścięgnistych limfocyty T o cechach komórek odporności wrodzonej oraz cytokiny: czynnik martwicy nowotworów (tumor necrosis factor -TNF), interleukiny 23, 17 i 22, biorą udział w tych lokalnych procesach patologicznych. Mechanizmy molekularne, które biorą udział w zapaleniu stawów, destrukcji chrząstki i kości stawowej, są podobne do tych w reumatoidalnym zapaleniu stawów i są zatrzymywane przez skuteczną terapię przeciwzapalną, w tym leki biologiczne neutralizujące TNF. Terapie anty-TNF jednak nie hamują patologicznego tworzenia kości, a to zjawisko jest cechą charakterystyczną SpA. Powoduje ono m.in. powstawanie syndesmofitów i ankylozę kręgosłupa. Mechanizmy molekularne leżące u podłoża patologicznej przebudowy kości w SpA, jak również ich interakcje ze szlakami zapalnymi nie są w pełni poznane. Trzy główne omówione w artykule hipotezy są próbą wyjaśnienia tego problemu. S u m m a r ySpondyloarthritis (SpA) is a form of chronic inflammatory arthritis affecting axial and peripheral joints, which may be initiated by inflammation of joint subchondral bone marrow or enthesitis. Invasive fibrous tissue which substitutes bone marrow, entheseal innate-like T lymphocytes and proinflammatory cytokines: tumor necrosis factor (TNF), interleukins 23, 17 and 22, all contribute to these local pathological processes. Joint inflammation, joint cartilage and bone destruction are mediated by mechanisms that are molecularly similar to rheumatoid arthritis. These pathologic processes are halted by effective anti-inflammatory therapy, including anti-TNF biological agents. By contrast, anti-TNF therapy fails to inhibit pathologic new bone formation, which is a unique hallmark of SpA and results, among others things, in syndesmophyte formation followed by spine ankylosis. The molecular mechanisms driving pathologic bone remodeling in SpA patients and interaction of this process with inflammatory pathways are not fully understood. Three hypotheses, discussed in the article, have been proposed to explain this issue.

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In Situ Analysis of Interleukin–23– and Interleukin‐12–Positive Cells in the Spine of Patients With Ankylosing Spondylitis

Cited by 130 publications

References 35 publications

MicroRNA let-7i induced autophagy to protect T cell from apoptosis by targeting IGF1R

MicroRNA let-7i induced autophagy to protect T cell from apoptosis by targeting IGF1R

Biomarkers, imaging and disease activity indices in patients with early axial spondyloarthritis: the Italian arm of the SpondyloArthritis-Caught-Early (SPACE) Study

New aspects of spondyloarthritis pathogenesis. Part III – arthritis, pathological bone remodeling

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