Tumour necrosis factor (TNF)-alpha and TNF-beta, also called lymphotoxin (LT), are bound by soluble truncated TNF receptors (sTNFRI and II) that are released from cell surfaces and act as natural inhibitors of TNF-induced inflammation. We investigated the plasma levels of sTNFRI and II in parallel with LT binding capacity (LTBC) in 44 patients with juvenile chronic arthritis (JIA).
LTBC was determined by spiking diluted plasma samples with 1000 pg/ml of human recombinant LT. Detectable LT was measured by an in-house ELISA and LTBC was expressed in arbitrary units (AU) as the percentage value of bound LT to added LT. The levels of sTNFRI and-II were measured by ELISA (R&D).
We found slightly reduced sTNFRI and II levels in JIA patients (n=44) compared with healthy controls sTNFRI: 1118 pg/ml (656-2074) [mean (range)] vs. 1262 pg/ml (819-2280) p=0.015; sTNFRII: 1953 pg/ml (889-4476) vs. 2311 pg/ml (1309-4186) p=0.008. The sTNFRI levels correlated positively with morning stiffness (r=0.30, p=0.044), physician's global assessment (r=0.39; p=0.009) and CRP (r=0.43; p=0.0048). sTNFRII did not correlate with measures of disease activity. In contrast, patient LTBC values were elevated compared to controls: 44 AU (36-52) vs. 31 AU (13-41) [mean (range)], p<0.0001, but did not correlate with disease activity.
Despite overall slightly reduced plasma levels of sTNFRI and II, the capacity to bind TNF appeared to be increased in plasma samples from JIA patients.