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The aim of this study was to evaluate prospectively cytokine levels and disease activity in juvenile idiopathic arthritis (JIA) patients treated with and without tumour necrosis factor (TNF)-α inhibitors. TNF-α inhibitor-naive JIA subjects were followed prospectively for 6 months. Cytokine levels of TNF-α, interleukin (IL)−1β, IL-6, IL-8, IL-10 and IL-17 were measured at baseline for JIA subjects and healthy controls (HCs). Cytokine levels were then measured at four time-points after initiation of TNF-α inhibition for anti-TNF-α-treated (anti-TNF) JIA subjects, and at two subsequent time-points for other JIA (non-TNF) subjects. JIA disease activity by Childhood Health Assessment Questionnaire (CHAQ) disability index/pain score and physician joint count/global assessment was recorded. Sixteen anti-TNF, 31 non-TNF and 16 HCs were analysed. Among JIA subjects, those with higher baseline disease activity (subsequent anti-TNFs) had higher baseline TNF-α, IL-6 and IL-8 than those with lower disease activity (non-TNFs) ( P < 0·05). TNF-α and IL-10 increased, and IL-6 and IL-8 no longer remained significantly higher after TNF-α inhibitor initiation in anti-TNF subjects. Subgroup analysis of etanercept versus adalimumab-treated subjects showed that TNF-α and IL-17 increased significantly in etanercept but not adalimumab-treated subjects, despite clinical improvement in both groups of subjects. JIA subjects with increased disease activity at baseline had higher serum proinflammatory cytokines. TNF-α inhibition resulted in suppression of IL-6 and IL-8 in parallel with clinical improvement in all anti-TNF-treated subjects, but was also associated with elevated TNF-α and IL-17 in etanercept-treated subjects. [ABSTRACT FROM AUTHOR]

CD3–CD56+dim natural killer (NK) cells, which are cytotoxic against virally infected cells, may be important in hepatitis C virus (HCV)-infected patients who are successfully treated with pegylated interferon (PEG-IFN)- α. We used flow cytometry to enumerate activated (CD69+) and apoptotic (annexin-V+) dim (CD3–CD56+dim) and bright (CD3–CD56+bright) NK cells obtained from HCV-infected patients before treatment ( n = 16) and healthy controls ( n = 15) in the absence and presence of pegylated interferon (PEG-IFN)- α-2b. A subset of HCV-infected patients, subsequently treated with PEG-IFN- α-2b in vivo, was determined to have a sustained virological response (SVR, n = 6) or to not respond (NR) to treatment ( n = 5). In the absence of IFN, activated dim (CD3–CD56+dim CD69+) NK cells were significantly decreased ( P = 0·04) while activated apoptotic dim (CD3–CD56+dimCD69+annexin-V+) NK cells tended to be increased ( P = 0·07) in SVR patients compared with NR patients. Activated bright (CD3–CD56+brightCD69+) and activated apoptotic bright (CD3–CD56+brightCD69+annexin-V+) NK cells were significantly correlated ( P = 0·02 and P = 0·01, respectively) with increasing hepatic inflammation. These findings suggest that in the absence of PEG-IFN, activated dim (CD3–CD56+dimCD69+) NK cell turnover may be enhanced in SVR compared with NR patients and that activated bright (CD3–CD56+brightCD69+) NK cells may play a role in liver inflammation. [ABSTRACT FROM AUTHOR]

The responses of fresh and frozen lymphocytes to mitogens and antigens have been compared using samples collected on five separate occasions from one normal donor. The day-to-day variation seen with the fresh cells was eliminated by the use of frozen cells. Thawed cells from one donor collected on one occasion hut studied on five separate occasions and compared to fresh cells on the same days showed fluctuations from day to day as well, confirming that the day-today variation seen is due to technical and not biological phenomena. Cryopreserved cells showed a decrease in responses to specific microbial antigens, a slight shift in the PHA dose-response curve, but no significant difference in responses to Con A or PWM. The relative proportion of lymphocyte subpopulations changed with freezing and thawing. The proportion of T cells increased slightly and the proportion of H cells decreased. [ABSTRACT FROM AUTHOR]