Content area

Full text

Sonja Dulic [1] and Zsófia Vásárhelyi [2] and Florentina Sava [2] and László Berta [3] and Balázs Szalay [4] and Gergely Toldi [2] and László Kovács [1] and Attila Balog [1]

Academic Editor: Tânia Silvia Fröde

1, Department of Rheumatology and Immunology, Faculty of Medicine, Albert Szent-Györgyi Health Center, University of Szeged, Szeged, Hungary, u-szeged.hu

2, First Department of Obstetrics and Gynecology, Semmelweis University, Budapest, Hungary, semmelweis.hu

3, First Department of Pediatrics, Semmelweis University, Budapest, Hungary, semmelweis.hu

4, Department of Laboratory Medicine, Semmelweis University, Budapest, Hungary, semmelweis.hu

Received Feb 14, 2017; Revised May 22, 2017; Accepted Jul 19, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Rheumatoid arthritis (RA) is the most common chronic autoimmune joint disease, which leads to progressive articular destruction without treatment [1]. The abnormal function of CD4+ and CD8+ cells plays a key role in the autoimmune process leading to the development of RA. This is reflected by a number of observations indicating that the proportion of different CD4+ subsets responsible for the harmonized immune response is skewed to a proinflammatory direction. The frequency of Th1, Th2 helper, and proinflammatory Th17 cells is increased [2, 3], while that of regulatory T-cells (Treg) is decreased in the peripheral blood of RA patients [4–7]. Biological therapies, including monoclonal antibodies targeting tumor necrosis factor-α (TNF) and interleukin-6 receptor (IL-6R), have emerged as disease-modifying agents with much higher therapeutic potential than conventional immunosuppressive therapies. Little is known about how the alterations in the T-cell subset composition are affected by anti-TNF or anti-IL-6R drugs. Few studies, including our previous examinations [7], followed T-cell subset prevalence changes, but in most of them, only short-term follow-up was evaluated [8–15]. As changes in cell numbers are supposed to require longer time, we presume that short-term follow-up may not be sufficient. Furthermore, the number of patients was not high enough to capture subtle changes in cell proportions; moreover, some studies were not homogenized for disease activity or response to therapy, or only few types of cells were monitored. Data on the effects of IL-6R blocker therapy are especially limited [16–18].

Our knowledge about the...
 
  

Show less