SUMMARYIn the present study, we evaluated the NK cell cytotoxic activity in a group of HCV-infected individuals. Although the number of NK cells present in the peripheral blood of the HCV-infected patients was comparable to non-infected individuals, spontaneous NK cytotoxicity was four-fold lower (P < 0 . 001) than in normal donors. This functional impairment was not overcome by depletion of adherent or B cells, and it was partially restored by short-term (18 h) stimulation with IL-2. However, long-term stimulation (72 h) with this lymphokine induced activated killer cell (LAK) activity comparable to normal controls. The reduction in NK cytotoxic response does not seem to be due to soluble suppressive factors, since incubation of normal peripheral blood mononuclear cells (PBMC) with infectious HCV serums for a 4-h period does not affect NK spontaneous cytotoxic activity. Successful in vitro infection of PBMC with HCV infectious serum also resulted in an impairment of NK cytotoxicity, suggesting that altered NK function is associated with HCV infection and may be responsible, at least in part, for the chronicity of the infection.

In patients with systemic lupus erythematosus (SLE) metabolic alterations are often observed, which may be due to either the disease, the genetic background or the treatment. We studied the serum levels of the adipokines leptin, adiponectin, resistin, visfatin and ghrelin in patients with SLE and controls. Leptin levels were lower and adiponectin, ghrelin and visfatin levels were higher in the patients. No significant differences were encountered for resistin. The values of adipokines were independent of treatment, even after correction for body mass index. Inverse correlations were found among leptin and adiponectin, ghrelin and visfatin. We conclude that adipokines are involved in the metabolic imbalance of patients with SLE.

Silent lupus nephritis (SLN) was investigated in 42 renal asymptomatic patients and compared with 49 untreated patients with overt lupus nephropathy (OLN). Urinary sediment, quantitative proteinuria, creatinine clearance, antinuclear antibodies (ANA), complement, circulating immune complexes (CIC) and renal biopsies were evaluated in all of the patients. Forty-one out of the 42 (97.6%) patients had SLN according to histopathological findings. Results showed that the mean age, female/male ratio and the clinical activity index (SLEDAI) were similar in both groups (P > 0.05). The prevalence of ANA, anti-ds DNA, anti-ENA autoantibodies and C4 serum levels showed no statistical differences between the two groups (P > 0.05). Conversely, in the OLN group, elevated CIC and diminished CH50 and C3 serum levels were significantly different (P < 0.01). WHO class II was the predominant renal lesion in the group with SLN (P < 0.0001), whereas class IV was in the OLN patients (P < 0.0001). We conclude that, in our series, SLN was highly prevalent in renal asymptomatic patients with otherwise systemic lupus erythematosus. Furthermore, abnormal levels of CIC, CH50 and C3 associated with WHO class II suggest a moderate but ongoing activation of immune-mediated renal injury mechanisms.

Utilizing the first and second generation of enzyme immunoassays which detect antibodies to the C virus we investigated the frequency of anti-HCV antibodies in 315 patients undergoing hemodialysis. Other subpopulations at risk were used as reference groups. One hundred and twenty-three samples (39%) from the hemodialysis group repeatedly showed anti-HCV positive antibodies while only 19% and 1% were positive in the reference groups. The rate of anti-HCV reactive patients correlated with time on hemodialysis (less than 1 year, 17%; 1 to 5 years 43%; greater than 5 years, 64%; r = 0.94, P less than 0.001) and with the number of blood transfusions (1 to 10, 40%; greater than 10, 76%; r = 0.97; P less than 0.001). Length of time on hemodialysis was shown to be the major risk factor in thirty-three anti-HCV positive patients who had no previous record of blood transfusions. Co-infection with HBV was demonstrated in 41% out of 123 anti-HCV reactive patients, and increased alanine aminotransferase (ALT) activity was documented in this co-infected group. Our results further extend the observations on the predisposing factors to HCV spread in hemodialysis units, and suggest that in these renal patients co-infection with C and B viruses is a major cause of rising ALT activity.

Antigammaglobulins, or rheumatoid factors, can be demonstrated in the sera of the majority of patients with rheumatoid arthritis (RA) by the agglutination of sensitized sheep red blood cells, bentonite, or latex particles coated with gammaglobulin (1-3). These tests provide only a semiquan- titative estimate of the amount of antigammaglobulins present and do not indicate the distribution of the antigammaglobulins among the different immunoglobulin classes.Rheumatoid factors (RF) were first described as 19s yM globulins (4, 5). Later RF were reco