T cell responses in psoriasis and psoriatic arthritis

Diani, Marco; Gf, Altomare; Reali, Eva

doi:10.1016/j.autrev.2014.11.012

Cited by 130 publications

(90 citation statements)

References 58 publications

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“…Prolonged inflammation leads to extensive joint damage, and therefore, early diagnosis and treatment is mandatory. T lymphocytes (T cells) play a key role in the pathogenesis of both psoriasis and PsA [4]. Activated T cells infiltrate the skin and stimulate keratinocytes to proliferate and produce interleukin-2 (IL-2) and other growth factors.…”

Section: Introductionmentioning

confidence: 99%

Analysis of Programmed Death-1 in Patients with Psoriatic Arthritis

et al. 2015

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Programmed death-1 (PD-1) is an inhibitory co-receptor that is highly expressed in T lymphocytes that has been shown to downregulate inflammatory responses in several inflammatory diseases including systemic lupus erythematosus and rheumatoid arthritis. Yet, the role of PD-1 in psoriatic arthritis (PsA) has not been studied. In order to fill this gap, we measured the expression levels of PD-1 in peripheral T cells from patients with active disease. Twenty patients and fifteen age-matched healthy control subjects were recruited. The percentage of CD3(+)PD-1(+) T cells was measured by flow cytometry. Despite normal concentration of peripheral T cells, the expression levels of PD-1 were significantly higher in patients compared to healthy controls. Interestingly, among the patients, the expression levels inversely correlated with disease activity measured by disease activity scores (DAS28). PD-1 expression levels strongly correlated with the number of tender and swollen joints, but not with C-reactive protein (CRP) levels or psoriasis area and severity index (PASI). Functionally, in vitro ligation of PD-1 receptor in PsA T cells inhibited interleukin-2 (IL-2) secretion, Akt phosphorylation, and Rap1 activation. These findings suggest that PD-1 might serve as a biomarker for disease activity in PsA and highlight the need for additional studies in order to establish the role of PD-1 in PsA pathogenesis.

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Section: Introductionmentioning

confidence: 99%

Analysis of Programmed Death-1 in Patients with Psoriatic Arthritis

et al. 2015

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“…ESpA pathogenesis, although initially linked to Th17, has been reported to be associated with innate like-T cell subpopulations that respond towards IL-23. These cells are present with a specific tissue distribution and could play a vital function in the development or progression of SpA-related pathology [33]. Moreover, there is evidence for increased IL-23 expression in inflamed tissues including the gut of SpA patients without an overt IBD [34].…”

Section: Enteropathic Spa: Insights On the Pathogenesismentioning

confidence: 99%

Impact of a multidisciplinary approach in enteropathic spondyloarthritis patients

Conigliaro

Chimenti

Ascolani

et al. 2016

Autoimmunity Reviews

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Spondyloarthritis (SpA) and inflammatory bowel disease (IBD) are chronic autoinflammatory diseases that partially share the genetic predisposition and the unchecked inflammatory response linking the gut to the joints. The coexistence of both conditions in patients and the increased cross-risk ratios between SpA and IBD strongly suggest a shared pathophysiology. The prevalence of Enteropathic-related Spondyloarthritis (ESpA) in IBD patients shows a wide variation and may be underestimated. It is well accepted that the management of joint pain requires rheumatological expertise in conjunction with gastroenterologist assessment. In this view, we aimed at assessing, in a prospective study performed in a combined Gastro-Intestinal and Rheumatologic "GI-Rhe" clinic: (1) the prevalence of ESpA and other rheumatologic diseases in IBD patients with joint pain; (2) the features of the ESpA population; and (3) the diagnostic delay and the potential impact of the combined assessment. From November 2012 to December 2014, IBD patients with joint pain referring to a dedicated rheumatologist by the IBD-dedicated gastroenterologist were enrolled. Clinical and biochemical evaluations, joint involvement and disease activity assessment, diagnostic delay, and treatment were recorded. IBD patients (n = 269) with joint pain were jointly assessed in the "GI-Rhe" Unit. A diagnosis of ESpA was made in 50.5% of IBD patients with joint pain. ESpA patients showed a peripheral involvement in 53% of cases, axial in 20.6% and peripheral and axial in 26.4% of cases. ESpA patients had a higher prevalence of other autoimmune extra-intestinal manifestations and received more anti-TNF treatment compared with IBD patients. A mean diagnostic delay of 5.2 years was revealed in ESpA patients. Patients with joint disease onset in the 2002-2012 decade had reduced diagnostic delay compared with those with onset in the 1980-1990 and 1991-2001 decades. Diagnostic delay was further reduced for patients with joint onset in the last two years in conjunction with the establishment of the GI-Rhe clinic. Multidisciplinary approach improved management of rheumatic disorders in IBD patients allowing a more comprehensive care.

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“…Possible role of mast cells and IL-37 in the pathogenesis of psoriasis @ C I C E d i z i o n i I n t e r n a z i o n a l i between keratinocytes and immune cells, such as Th1, Th17, Th22, B cells, macrophages and MCs (13). Activated T-cell subsets, localized in the skin, initiate a local inflammatory process leading to development of a psoriatic plaque (14).…”

Section: Reviewmentioning

confidence: 99%

Possible role of mast cells and IL-37 in the pathogenesis of psoriasis

Conti¹

2017

cderm

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T cell responses in psoriasis and psoriatic arthritis

Cited by 130 publications

References 58 publications

Analysis of Programmed Death-1 in Patients with Psoriatic Arthritis

Analysis of Programmed Death-1 in Patients with Psoriatic Arthritis

Impact of a multidisciplinary approach in enteropathic spondyloarthritis patients

Possible role of mast cells and IL-37 in the pathogenesis of psoriasis

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