Impaired function of regulatory T-cells (Treg) leads to a failure in immune tolerance and triggers autoimmunity. We analyzed whether the deficiency in Treg in systemic lupus erythematosus (SLE) is accompanied by an increase in effector T-cell responses. We studied the frequencies of IL-17A (Th17) and IFNg (Th1) producing CD4 + T-cells by flow cytometric detection of intracellular cytokines in PMA/ionomycin stimulated blood lymphocytes from seven patients with active SLE, eight with SLE in remission, and 11 healthy controls. Circulating Treg were evaluated as CD4 + CD25 + lymphocytes expressing FoxP3. There was no difference in the percentage of Treg cells between the groups, but their absolute counts were decreased in active SLE (5 [1-7] cells/μL) compared to inactive SLE (11 [6][7][8][9][10][11][12][13][14][15]; p = 0.05) and healthy controls (16 [10-20]; p < 0.01). Both the frequency and numbers of Th1 cells were decreased in SLE compared to controls. No difference was observed in the number of Th17 cells, which resulted in a decreased Th1/Th17 ratio. In parallel, a higher Treg/Th17 ratio in healthy controls (2.2 [1.8-3.6]) compared to active SLE (1.1 [1.0-2.1]; p < 0.05) was observed. There was a correlation between the number of Treg cells and disease activity status (SLEDAI, r = -0.59). SLE patients in the active phase of the disease are characterized by a deficiency in Treg cells and decreased Treg/Th17 ratio. This suggests that the imbalance between major T-cells subsets might be responsible for an increased proinflammatory response in the exacerbation
We performed a double-blind, crossover, placebo-controlled study on the effect of fluticasone propionate (FP) treatment on chronic eosinophilic rhinosinusitis in 15 patients with aspirin-induced asthma (AIA). There were 10 women and five men aged 32-60 years; average: 45 years. After a 10-day run-in period, patients underwent two 4-week treatment courses (FP vs placebo), separated by a 2-week washout interval. Clinical activity of FP was evaluated by daily measurement of peak nasal inspiratory flow (PNIF) and a scoring system of subjective symptoms. Nasal challenges with E-lysine aspirin, using active anterior rhinomanometry, were performed at the entry and on the last day of each treatment period. Weekly mean values of symptom scores were generally lower and PNIF measurements higher during treatment with FP than with placebo. This difference was statistically significant for most recorded parameters for the whole 4-week FP treatment. On average, the reactions evoked by aspirin nasal challenge were significantly shorter and milder after treatment with FP than with placebo. In 8/13 patients, FP completely prevented aspirin-precipitated nasal reaction, whereas protection after placebo was observed in only 2/12 subjects (P = 0.004). We conclude that intranasal FP is an effective therapy for chronic eosinophilic rhinitis in patients with AIA.
Conventional risk factors of coronary artery disease fail to explain the increased frequency of cardiovascular morbidity in patients with systemic lupus erythematosus (SLE). The study was conducted to determine possible association between the heart structure and function abnormalities with established prognostic value assessed by non-invasive imaging techniques and markers of autoimmune and inflammatory phenomena typical for SLE. Echocardiography and single photon emission computerized tomography (SPECT; Tc-99m-MIBI) at rest were performed in 60 SLE patients in a stable clinical condition of their disease. Laboratory evaluation included serum levels of C-reactive protein (CRP), complement C3c and C4 components and antiphospholipid antibodies (aPL). The latter included serum anticardiolipin (aCL) and anti-β2-glycoprotein I (antiβ2GPI) antibodies, both of IgG and IgM class, and lupus anticoagulant (LA) in plasma. Echocardiography revealed pathologic thickening of valvular leaflets and/or pericardium in more than 60% of patients. Right ventricular systolic pressure (RVSP) was elevated (>30 mmHg) in 16.7%. Myocardial perfusion defects were present in 36.7% of patients, despite normal ECG recordings and a lack of clinical symptoms of myocardial ischaemia. There was a significant association between thickening of valvular leaflets and/or pericardium and high CRP and low C3c and C4 concentrations. On the other hand, increased RVSP and the presence of myocardial perfusion defects were associated with the presence of anticardiolipin and antiβ2GPI antibodies of the IgG class. Increased anticardiolipin IgG levels predicted perfusion defects in SPECT study with 100% sensitivity and 68% specificity, whereas elevated antiβ2GPI IgG levels predicted RVSP elevation (>30 mmHg) with 100% sensitivity and 78% specificity. In stable SLE patients pericardial and valve abnormalities may be associated with markers of an ongoing inflammation. Also, pulmonary systolic pressure elevation and myocardial perfusion defects are combined with elevated levels of anticardiolipin and antiβ2GPI antibodies of the IgG class. These results indicate that even clinically silent pulmonary hypertension and myocardial perfusion defects in SLE patients could be causally related to the presence of antiphospholipid antibodies.
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