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Biomedical subjects

E Taccari

Publications and source records attributed to E Taccari.

At least 55 records · Page 3Linked to original sources

[The role of interleukin-12 in immune-mediated rheumatic diseases].

OBJECTIVE: IL-12 is a proinflammatory cytokine produced by different antigen presenting cells. It has been shown to exert a critical role in inducing Th1 phenotype, thus initiating cell-mediated immune responses, but the significance of IL-12 in rheumatic diseases is not clear. Aim of the study was to determine IL-12 serum levels in immune rheumatic diseases and to analyse the relationship of this cytokine with main clinical and laboratory parameters. METHODS: We analysed, by ELISA, serum IL-12 levels in 114 patients with SLE, 47 with SS, 32 with SSc, 84 with RA, 138 with PA and in 17 healthy controls. We also examined main clinical and laboratory parameters, including autoantibody profile and clinical indices of disease activity. RESULTS: IL-12 serum levels were significantly higher in SLE and SS patients respect to controls. IL-12 serum levels were significantly higher in SLE patients compared to those affected by RA, PA and SSc. When we evaluated disease activity in SLE patients, we found significantly higher IL-12 serum levels in subjects with fever or in those without renal involvement, while no correlation was found in the other rheumatic immune diseases. CONCLUSIONS: These findings suggest that IL-12, modulating cell and humoral immune responses, is involved in the pathogenesis of immune rheumatic diseases, such as SLE and SS.

Adolescent↗

[Anti-tissue transglutaminase antibodies in inflammatory and degenerative arthropathies].

Recent studies identified tissue transglutaminase (tTG) as the antigen eliciting antiendomysial antibodies (EMA) in celiac disease (CD). Anti-tTG antibodies have therefore been proposed as a serological test for CD. Nevertheless, IgA anti-tTG but not EMA have also been found in inflammatory bowel disease patients, suggesting that these antibodies are linked to a tissue lesion rather than to an auto-immune component of CD. To confirm this hypothesis, we evaluated the presence of IgA anti-tTG in patients with inflammatory and degenerative diseases, in whom tissue lesions presented far away from the intestinal mucosa. The study was carried out on the serum and synovial fluid (SF) of 68 patients with rheumatoid arthritis (RA=33), psoriatic arthritis (PsA=26) and osteoarthritis (OA=9). In RA, PsA and OA sera, IgA anti-tTG were positive in 33%, 42% and 11% of patients, respectively. Serum anti-tTG levels were significantly higher in RA (p<0.0001), PsA (p<0.0001) and OA (p<0.02) with respect to healthy controls. SF anti-tTG levels were significantly higher in PsA (p<0.018) than in OA. A good correlation between serum and synovial fluid anti-tTG levels was found in all arthropathies This study suggests that tTG is not the only antigen of EMA and, furthermore, that IgA anti-tTG antibodies represent a general lesion-associated event. Moreover, the significant correlation between serum and synovial fluid anti-tTG levels allow us to hypothesise that these antibodies could be synthesized in the site of arthritic lesions.

Adolescent↗

[Role for familial and genetic features in the therapeutic response of psoriatic arthritis].

AIM OF THE STUDY: To analyze PsA patients with and without a familiar distribution for Ps and PsA, in order to better evaluate the genetic data, to verify the existence of different expression of the disease and finally to define the susceptibility to treatment in these patients. MATERIALS AND METHODS: 230 PsA patients were selected for familiar or sporadic distribution of the disease and were evaluated for the main clinical, demographic, radiological and laboratory features, as well as for the ongoing treatments. In each patient HLA class I (A,B,C) and II (DRB1, DQB1) antigens were typed with PCR-SSP method while MICA-A exon 5 microsatellite typing was performed by heteroduplex analysis in 122 subjects. RESULTS: A familiar distribution for Ps and PsA was found in 68 patients (29.6%) although only two patients had familiarity for PsA. In the familiar PsA group the male prevalence was significantly higher respect to the sporadic one (p<0.001) and the more frequently involved relative was the father (28%). Mean age (p<0.006) and age at onset of Ps (p<0.004) and PsA (p<0.014) were significantly lower in familiar respect to sporadic PsA. Between the two groups no difference was found concerning the articular involvement, the radiological findings, the disease activity (including number of painful/swollen joints), the inflammatory laboratory parameters (including ESR and CRP) and genetic aspects, including the frequencies of MICA-A alleles that were analysed in 30 patients with the familiar form and in 92 with the sporadic one. In the follow-up the therapeutic response to any evaluated treatment adopted for PsA did not show any significant difference in the two groups. All these results were confirmed even when the patients in the two groups were matchable for sex, age and disease duration. CONCLUSION: Our results confirm that familiar PsA is characterized by an early onset of the disease and by a male and fatherly predominance respect to the sporadic form, although the clinical-radiologic findings, the genetic typing and the therapeutic response do not permit us to identify any particular subset.

Adolescent↗

Immunohistologic markers of immune activation and changes of glycosylation of serum proteins in primary Sjögren's syndrome.

OBJECTIVE: [corrected] To assess the possible correlations between the immune activation of certain surface antigens at the lip salivary gland (LSG) level, and changes in glycosylation of serum proteins in primary Sjögren's syndrome (SS). METHODS: LSG biopsy samples were obtained from 22 SS patients (mean age 56.3 years; mean disease duration 70.8 months) and prepared for immunohistochemical analysis using murine monoclonal antibodies for interleukin-2 receptor (IL-2R) (CD25) and for the class II major histocompatibility antigen HLA-DR. The glycosylation of serum proteins was evaluated in all patients by an enzyme-linked lectin assay (ELLA) using concanavalin A (Con A). RESULTS: In LSG specimens the presence of IL-2R was observed at the infiltrating level, mainly periductally, in 13 (59%) cases and on the epithelial cells of 14 (64%) patients. In 13 out of 22 SS patients (59%) a marked positivity both of the infiltrates and of the epithelium was found for anti-HLA-DR monoclonal antibody. The degree of expression of different antigens on LSG samples was correlated with their histologic class according to Tarpley evaluation. The positivity for IL-2R and HLA-DR molecules on glandular tissues was correlated. A significant increase in the total Con A reactivity of serum proteins was found in those patients expressing IL-2R and HLA-DR antigens on LSG specimens. CONCLUSIONS: The co-expression of IL-2R and HLA-DR antigens on both the epithelium and infiltrates of LSG is consistent with a participation of these cells in the immune process of SS. Moreover, changes in the glycosylation of serum proteins seem to be related to the presence of these immunoactivation markers of the disease at the LSG level, suggesting that the control of protein glycosylation could be mediated by the same mechanisms involved in the tissue damage of SS.

Adult↗

Interleukin-13 in autoimmune rheumatic diseases: relationship with the autoantibody profile.

OBJECTIVE: Several cytokines play a role in the production of autoantibodies such as RF and ANA by B-lymphocytes; the role of IL-13 in this process has not been previously studied. We investigated the relationship between the serum concentration of this cytokine and circulating autoantibodies. METHODS: IL-13 serum levels, as well as RF and ANA, were evaluated in 282 patients with autoimmune rheumatic diseases including RA (n=84), SLE (n= 114), SS (n=52) and Scl (n=32). RESULTS: Serum levels of IL-13 (pg/ml) were significantly higher in patients with RA (p < 0.00003), SLE (p < 0.03), SS (p < 0.0007), or Scl (p < 0.025) compared to controls. IL-13 serum levels correlated with those of RF in RA (p < 0.00001), SLE (p < 0.003) and Scl (p < 0.03). IL-13 levels were higher in RA (p<0.0003), SLE (p<0.005) and Scl (p<0.05) patients with RF than in patients without RF. SS patients with antiSSA/Ro antibodies had significantly higher IL-13 levels than SS patients without this autoantibody (p < 0.04). No statistically significant correlation was found between IL-13 levels and any other antinuclear autoantibody, total immunoglobulin levels or the main clinicalfeatures of each disease. CONCLUSION: The evidence of higher IL-13 levels in our RA, SLE, SS and Scl patients confirms that this cytokine is involved in the pathogenesis of autoimmune rheumatic diseases. The relationship of this cytokine with RF in RA, SLE and Scl, as well as with antiSSA/ Ro antibody in SS, strengthens the hypothesis that it plays a role in autoantibody production. However, the different autoantibody synthesis by B-cells recognises different pathways depending on the underlying autoimmune disease.

Adolescent↗

Natural killer cells and gamma/delta T cells in synovial fluid and in peripheral blood of patients with psoriatic arthritis.

OBJECTIVE: NK surface markers and gamma/delta TCR antigen are involved in non-MHC-restricted cytotoxicity, which represents a major effector mechanism of the cell-mediated immune response. We evaluated in PsA patients SF and PB lymphocytes expressing these cellular subsets in order to obtain information on the possible role played by them in the disease. METHODS: We studied 29 PsA and 27 RA patients, as well as 27 healthy controls. In 17 PsA and 16 RA patients with knee joint effusion, analysis of SF was performed. SF and PB lymphocyte analysis was performed by direct dual immunofluorescence flow cytomettry using anti-CD3, anti-CD4, anti-CD8, anti-CD19, anti-TCR-gamma/delta-1 and anti-CD16 and anti-CD56 monoclonal antibodies. RESULTS: PsA and RA patients had, with respect to controls, lower values (both as percentages and in absolute numbers) of PB T cells expressing gamma/delta TCR. SF Iymphocytes of PsA and RA patients were characterised, as compared to PB lymphocytes, by lower numbers (both in absolute numbers and in relative terms) of NK and NK-T cells. Considering the absolute numbers of the various lymphocyte subsets, a strong correlation was found in PsA SF between gamma/delta T cells and NK (p < 0.0007) or NK-T cells (p < 0.0003), as well as between NK and NK-T cells (p < 0.0019). There was instead no statistically significant correlation among the different SF or PB lymphocytes and the most relevant clinical or serological parameters. CONCLUSION: This study, analyzing the impairment of different subsets involved in non-MHC-restricted cytotoxicity, suggests that this component of the cell-mediated immune response seems to play a pivotal role in the development of PsA.

Adolescent↗

[Chyliform effusions in rheumatoid arthritis. Cytochemical and ultrastructural studies of the foam cells].

The authors studied the cell composition and the cytochemistry and ultrastructure of the frothy cells in two periarticular chyliform effusions in rheumatoid arthritis. Compared with the polymorphonuclear cells, the mononuclear cells were very numerous with many frothy cells. Cholesterol crystals, identified by X-ray diffraction, were detected in fluids by polarised light, but only cytochemically and with the transmission electron microscope in the spumous cells. The latter contained not only neutral fat, but also hydrophobic lipids and phospholipids, but no cholesterol esters. A theory has been advanced that once phagocytosis has been accomplished, cholesterol crystal metabolism is not rapid and is too insufficient for cholesterol or its esters to accumulate in the cytoplasm. The polymorphonuclear leukocytes play only a small role in the phagocytosis of crystals and this probably plays a role in the absence of acute inflammation in structures which contain chyliform effusions.

Aged↗

Magnetic resonance imaging (MRI) of the brain in SLE: ECLAM and SLEDAI correlations.

Twenty-one unselected SLE patients were examined with Magnetic Resonance Imaging (MRI) for cerebral areas of high signal intensity (HSI). Nine patients (42.9%) had HSI and 6 (28.6%) had large (> or = 6 mm) lesions suggestive of cerebral involvement. Despite the lack of correlation among these lesions and clinical or immunological features, the SLEDAI and ECLAM indices were correlated to the number of large lesions (p < 0.002). Our findings suggest that brain MRI may be useful in the evaluation of SLE patients, not only those with evident neurologic symptoms, but also asymptomatic subjects with high disease activity indices.

Adolescent↗