T cell derived cytokines in psoriatic arthritis synovial fluids

Partsch, G; Wagner, Ernst; Leeb, Burkhard F.; Bröll, H; Dunky, Attila; Smolen, Josef S.

doi:10.1136/ard.57.11.691

Cited by 74 publications

(54 citation statements)

References 13 publications

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“…It has been shown that keratinocytes in psoriatic lesions resist apoptosis and have prolonged survival (12). In addition, IFN-y induces macrophages to release high levels of other inflammatory cytokines including TNF-a which are present at higher levels in psoriatic plaques and in the synovial fluid of patients with psoriatic arthritis (13)(14). The IL-2 receptor, CD25, is up-regulated on T cells within psoriatic lesions (15)(16).…”

Section: Discussionmentioning

confidence: 99%

Serum Cytokines and Bioumoral Immunological Characterization of Psoriatic Patients in Long Term Etanercept Treatment

Cordiali‐Fei

Ardigò

Mastroianni

et al. 2008

Int J Immunopathol Pharmacol

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The purpose of this study is to evaluate blood cytokines and immunological parameters in psoriatic patients during long-term treatment with etanercept. Forty-five subjects of both sexes affected by psoriasis with or without arthritis entered the study and were treated with etanercept according to international standard protocols. Biochemical blood analysis was carried out at baseline and during follow-up every second month. In particular, the following parameters were kept under control: antinuclear antibodies, anti-nDNA antibodies, anti-histone antibodies, blood cell count, circulating lymphocyte subtypes (CD3, CD4, CD8, CD16, CD19) and IgE. Cytokine profiles (IL-1-α, IL-1-β, IL-6, IL-8, IL-10, IL-12, INF, TNF- α) were also evaluated in blood samples during the treatment up to 1 year of follow-up. A significant decrease in PASI score (p<0.01) and in several cytokine levels was observed, particularly in IL-1, IL-6, IFN-γ (p<0.01) and to a lesser extent in TNF-α (p<0.05). No statistically significant changes were recorded after 1 year of follow-up in blood immunological parameters, in particular in ANA titre, CD4/CD8 ratio, IgE levels, CD16, CD19 and eosinophils count. In conclusion, long-term treatment with etanercept leads not only to a significant improvement in PASI score, but also to significant changes (reduction) in several proinflammatory and modulatory cytokines involved in the pathogenesis of the disease; on the other hand, there are no effects on immunological or bioumoral parameters showing that etanercept modulates rather than suppresses the physiological responses during psoriasis treatment.

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Section: Discussionmentioning

confidence: 99%

Serum Cytokines and Bioumoral Immunological Characterization of Psoriatic Patients in Long Term Etanercept Treatment

Cordiali‐Fei

Ardigò

Mastroianni

et al. 2008

Int J Immunopathol Pharmacol

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“…This notion is based on the presence of T lymphocytes in early psoriasis lesions (16), the beneficial effects of T lymphocyte-targeted therapies such as cyclosporin A (8), and the altered relationship between psoriatic keratinocytes and interferon-␥ (IFN␥) compared with normal keratinocytes (17). Data on the role of T cells in PsA are limited, but it has been suggested that they play a central role in its pathogenesis as well (18)(19)(20).…”

mentioning

confidence: 99%

Alefacept treatment in psoriatic arthritis: Reduction of the effector T cell population in peripheral blood and synovial tissue is associated with improvement of clinical signs of arthritis

Kraan

Kuijk

Dinant

et al. 2002

Arthritis & Rheumatism

135

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Objective. To investigate whether alefacept (a fully human lymphocyte function-associated antigen 3 [LFA-3]/IgG1 fusion protein that blocks the LFA-3/CD2 interaction) is able to reduce the signs and symptoms of joint inflammation in patients with active psoriatic arthritis (PsA).Methods. Eleven patients with active PsA were treated with alefacept for 12 weeks in an open-label and explorative study. Clinical joint assessment and laboratory assessments were performed at baseline and after 4, 9, 12, and 16 weeks of treatment. Serial synovial tissue (ST) biopsy specimens from an inflamed index joint (knee, ankle, wrist, or metacarpophalangeal joint) were obtained by arthroscopy at baseline and after 4 and 12 weeks of treatment.Results. At the completion of treatment, 6 of 11 patients (55%) fulfilled the Disease Activity Score (DAS) response criteria. Nine patients (82%) fulfilled the DAS response criteria at any point during the study. There was a statistically significant reduction in CD4؉ lymphocytes (P < 0.05), CD8؉ lymphocytes (P ‫؍‬ 0.05), and CD68؉ macrophages (P < 0.02) in the ST after 12 weeks of treatment compared with baseline. The ST and peripheral blood of those patients fulfilling the DAS response criteria contained more CD45RO؉ cells at baseline and displayed a significant reduction in these cells compared with nonresponding patients.Conclusion. The changes in ST, together with the improvement in clinical joint scores, after treatment with alefacept support the hypothesis that T cell activation plays an important role in this chronic inflammatory disease. Furthermore, since alefacept, a T cellspecific agent, led to decreased macrophage infiltration, the data indicate that T cells are highly involved in synovial inflammation in PsA.

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“…Considerable evidence implicates T cells in the pathogenesis of psoriatic arthritis as well as psoriasis. This includes the presence of T cells at sites of inflammation, the response of the disease to therapy directed at T cells, and the association of disease susceptibility with certain HLA alleles (1)(2)(3)(4)(5)(6). In particular, the specific importance of CD8 lineage T cells in the pathogenesis of psoriatic arthritis (7) is emphasized by three observations.…”

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confidence: 99%

Psoriatic Arthritis Joint Fluids Are Characterized by CD8 and CD4 T Cell Clonal Expansions that Appear Antigen Driven

Costello

Winchester

Curran

et al. 2001

The Journal of Immunology

110

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The CD8 αβT cell receptor repertoire in joint fluid of individuals with active psoriatic arthritis contained an average of 32 major oligoclonal expansions in many variable genes of the TCR β chain (BV) families, as shown by β-chain CDR3 length analysis. Interestingly, a small number of oligoclonal expansions were shared between simultaneous samples of joint fluid and blood; however, most expansions found in joint fluid were not identifiable in blood emphasizing the immunologic specificity of the clonal events for the inflamed joint at a given point of time. The CD4 T cell joint fluid repertoire contained fewer and smaller oligoclonal expansions also largely restricted to the joint, suggesting that CD4 T cells participate perhaps by interacting cognitively to generate the CD8 clones. The inferred amino acid sequence of a single CD8 oligoclonal expansion revealed that they usually are composed of one or a few structurally related clones at the amino acid sequence level with β-chains that encode identical or highly homologous CDR3 motifs. These were not shared among patients. Moreover, several clones that encoded the same amino acid sequence were found to be structurally distinct at the nucleotide level, strongly implying clonal selection and expansion is operating at the level of specific TCR-peptide interactions. The findings support a model of psoriatic arthritis inflammation involving extensive and selective Ag, likely autoantigen, driven intra-articular CD4, and CD8 T cell clonal expansions.

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T cell derived cytokines in psoriatic arthritis synovial fluids

Abstract: (Ann Rheum Dis 1998;57:691-693)

Cited by 74 publications

References 13 publications

Serum Cytokines and Bioumoral Immunological Characterization of Psoriatic Patients in Long Term Etanercept Treatment

Serum Cytokines and Bioumoral Immunological Characterization of Psoriatic Patients in Long Term Etanercept Treatment

Alefacept treatment in psoriatic arthritis: Reduction of the effector T cell population in peripheral blood and synovial tissue is associated with improvement of clinical signs of arthritis

Psoriatic Arthritis Joint Fluids Are Characterized by CD8 and CD4 T Cell Clonal Expansions that Appear Antigen Driven

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