[show abstract][hide abstract] ABSTRACT: Hepatitis C virus (HCV) is one of the most important etiologic agents of postransfusional hepatitis and a common cause of chronic hepatitis, cirrhosis and hepatocarcinoma. T helper (Th)17 cells are a newly discovered Th cell subset with implications in both host defense and autoimmunity. Th17 implications in chronic HCV infection are not well characterized. Given the important role in multiple other immune and inflammatory conditions, they are of obvious interest. Specific HCV-Th17 cells are implicated in immune response modulation, correlated with fibrosis severity and intrahepatic inflammatory status. Serum IL-17 levels are higher in chronic HCV infected patients and Th17 cytokines are modulated within the therapeutic response at anti-viral treatment. However, novel intriguing data indicate that Th17 boost could be associated with spontaneous HCV clearance. It is possible that Th17 could play a dual role (both beneficial and harmful) and that an unbalance of regulating factors (chemokines, transcription factors, receptor expression, etc.) rather than the lymphocyte itself could tip the Th17 immune response one way or another. The role of Th17 cells in host anti HCV defense is beginning to emerge and one has to focus upon its potential beneficial aspects and not only on its destructive potential.
Romanian journal of internal medicine = Revue roumaine de médecine interne 01/2012; 50(1):13-8.
[show abstract][hide abstract] ABSTRACT: HCV (hepatitis C virus) chronic hepatitis has become one the most expensive diseases for public health systems all over the world in the past 10-20 years, a real epidemic, the second most frequent, after hepatitis B virus infection. Due to the complex manifestations, one may consider HCV infection as a "systemic" disease. Mixed cryoglobulinemia (MC) is the most common extrahepatic manifestation of HCV infection, but cryoglobulinemic vasculitis (CV) is considered to be relatively sparse although prevalence studies are needed. Presence of serum cryoglobulins is essential for MC diagnosis, but serum levels do not correlate with the disease activity or prognosis. MC can be defined as a B lymphocyte proliferation disease being characterized by polyclonal activation and antibody synthesis. Evolution to lymphoma should be considered continuous but also other infectious, environmental or genetic factors could be involved. The t (14.18) translocation and Bcl-2 activation in B lymphocytes, B cell-activating factor (BAFF), E2-CD81 interaction, immunoregulatory T CD4+CD25(high) + lymphocytes and type III IFNs might play an important role in MC and lymphoma evolution in HCV patients.
Romanian journal of internal medicine = Revue roumaine de médecine interne 01/2011; 49(1):3-10.
[show abstract][hide abstract] ABSTRACT: Lupus erythematosus (LE) is an autoimmune inflammatory disease that involves many organs and systems. Immunological factors seem to play a key-role in LE pathogenesis. LE patients have T lymphocytes dysfunctions.Th17 is implicated in the pathogenesis of various autoimmune diseases like psoriasis, multiple sclerosis or rheumatoid arthritis. The purpose of this study was to evaluate the circulating Th17 cell population in LE patients.
A total of 15 LE patients were recruited and divided into three groups: systemic lupus erythematosus (SLE), discoid lupus (DLE) and subacute lupus (SCLE). Serum IL-17A, IL-17F and IL-23 were detected. Th17 circulating cells were evaluated by flow cytometry.
Serum IL-17A and IL-17F levels were higher in SLE, DLE and SCLE patients compared to healthy controls. The number of Th17 cells were higher in SLE and DLE patients (p<0.05). the number of CD3+IL-17+ cells were higher in SLE, DLE and SCLE patients (p<0.05).
Th17 lymphocytes are implicated in LE pathogenesis. Our findings suggest that IL-17 is implicated not only in SLE but also in DLE and SCLE immunopathogenesis.
Romanian journal of internal medicine = Revue roumaine de médecine interne 01/2010; 48(3):255-9.
[show abstract][hide abstract] ABSTRACT: Lupus erythematosus (LE) has a broad clinical spectrum from exclusively skin damage (chronic discoid lupus-DLE or subacute lupus erythematosus-SCLE) to systemic, multiorgan disease (involving skin, joints, kidney, central nervous system). LE is characterized by an autoimmune component. SCLE is characterized by erythemato-squamous lesions mainly in photoexposed areas. Apoptosis (programmed cellular death) is essential for normal embryogenesis and for normal tissue homeostasis and control. Inefficient apoptotic cell clearance has been correlated with inflammatory diseases and autoimmunity outburst. This study evaluates histological and immunohistochemical expression ofpro-apoptotic markers in patients with SCLE.
20 patients with SCLE and 10 healthy controls were selected. Biopsies from skin lesions were performed. Biopsies were evaluated for immunohistochemical expression of caspase 3, CD25, CD35, CD21, CD36, CD68, CD31, IgM detection, T and B cell markers.
In the inflammatory cells population we distinguished T lymphocytes, rare B lymphocytes, dendritic cells and macrophages. Within the lymphocyte population IL-2 receptor (CD25) expression was low but caspase 3 expression was intense in lymphocytes, epithelial cells and pericytes. Basal epithelial vacuolations were common. Phagocytic-cell and lymphocytic expression of CD35 (complement receptor 1-CR1) and CD21 (complement receptor 2-CR2) were lower when compared to healthy controls.
In SCLE patients we observed lymphocytic, epithelial and pericytal cell apoptosis and CR1 and CR2 expression are lower in professional phagocytes, suggesting a delay in the uptake of apoptotic bodies.
Romanian journal of internal medicine = Revue roumaine de médecine interne 01/2010; 48(3):261-5.
[show abstract][hide abstract] ABSTRACT: Autoantibodies against C1q are strongly linked to immune-complex disorders like systemic lupus erythematosus (SLE). Although anti-C1q antibodies have received much interest in the recent years, their biological functions remain unclear. Anti-C1q antibodies are strongly associated with lupus nephritis. Recent studies describe apoptosis as a key player in LE pathogenesis and C1q is an important opsonin, playing a central role in the uptake of apoptotic blebs. The aim of this study was to evaluate serum anti C1q antibodies, C1q with circulating immune complexes and correlation between serology and cutaneous apoptosis in patients with cutaneous lupus erythematosus.
79 subjects were recruited and divided into 4 groups-13 healthy controls, 26 with discoid chronic lupus (DLE), 23 with systemic lupus erythematosus (SLE) and 17 with subacute lupus erythematosus (SCLE). Blood samples and skin punched-biopsy specimens were performed. Serum anti-C1q antibodies and C1q associated to the immune complexes concentrations were determined by ELISA. Cutaneous caspase-3 expression was evaluated by immunohistochemistry.
SLE and SCLE patients had significantly higher levels of anti-C1q antibodies and serum C1q-CIC levels when compared to healthy controls (p < 0.05). Serum anti-C1q antibodies correlated with proteinuria in SLE patients (p < 0.05). Anti C1q antibodies levels also correlated with cutaneous caspase 3 expression in SLE and SCLE patients (both p < 0.05).
Anti C1q antibodies might play a pathogenic role in SCLE pathogenesis and being positively associated with cutaneous apoptosis markers might be associated with a negative prognosis and secondary SLE development.
Romanian journal of internal medicine = Revue roumaine de médecine interne 01/2010; 48(2):159-63.
[show abstract][hide abstract] ABSTRACT: The level of plasma lipid peroxidation was followed up in 66 patients with systemic vasculitides with autoimmune pathogeny (SLE and SV) treated with corticoid compounds. The effect of vitamin E associated to this treatment was also studied. The change of the redox cycle, of the red cell glutathione, and of the glutathione peroxidase activity, an enzyme supplying antioxidant protection, were studied in parallel. The results obtained demonstrated: an increased level of lipid peroxidation in the patients treated with corticoid substances, an increase that can be explained by the dyslipidemias induced by these compounds; a decrease of the red cell G-SH concentration owing to the continuous oxidative stress in this group of diseases. This decrease was associated with a concomitant increase of oxidated glutathione. The decrease of GSH, a substrate for glutathione peroxidase, induces an inhibition of this enzyme activity. The GSH/GSSH ratio may represent a useful marker of the evolution of disease. Administration of vitamin E in association with corticotherapy has a relatively reduced effect due to the complex metabolic disturbances with a continuous character in the autoimmune pathogenic processes. The chronic disturbance of the oxidants-antioxidants balance in patients with systemic vasculitides seems to create favourable conditions for the early onset of a process of atherogenesis with severe vascular effects.
Romanian journal of internal medicine = Revue roumaine de médecine interne 01/1994; 32(4):283-9.