Th17 cells are restrained by Treg cells via the inhibition of interleukin‐6 in patients with rheumatoid arthritis responding to anti–tumor necrosis factor antibody therapy

Abstract

Objective. The importance of interleukin-17 (IL-17

A Prospective Study on Inflammatory Cytokines and Bone Metabolism Mediators in Patients Affected by Rheumatoid and Psoriatic Arthritis treated with Adalimumab

“…In accordance with data from literature, higher levels of BAP were noticed in both RA and PsA patients compared with healthy controls, pointing out its involvement in periarticular bone changes [36,37]. In this context, correlation with SF IL-6 levels was shown supporting the local production of BAP in RA joints previously reported, suggesting that local BAP production might occur in the arthritic joints [38]. Furthermore, in PsA BAP was positively correlated with OPG levels.…”

Rheumatoid Arthritis: Prospects for Stopping the Runaway Train by Reintroduction of Tolerance

“…This affect was exerted through monocyte derived IL-6. Interestingly, they observed this Treg suppression only in patients on the anti TNF-α monoclonal antibody adalimumab, and not with the TNF receptor fusion protein, etanercept [87]. Increased Tregs and decreased Th17 cells have also been reported in RA patients treated with the anti IL-6 antibody tocilizumab [88].…”

Reply

“…RA-associated ILD has a major impact on mortality and morbidity among RA patients (3,4). As correctly stated by Conway et al, distinguishing MTX-induced lung toxicity from RA-associated lung disease is vital.…”

“…This question applies not only to TCZ, but also to other biologic agents such as infliximab or adalimumab, which have been shown by us and others to increase Treg cell frequencies both in the peripheral blood of RA patients (3,4) and in a mouse model of RA (5). Nevertheless, the study of Treg cells after administration of targeted treatments, focusing on the detection of a "hyperregulatory" T cell population, could provide valuable tools to predict response and resistance to biologic therapy in RA.…”