Mononuclear Phagocytes in Rheumatoid Arthritis Patients and their Relatives – Family Similarity
Marina I Arleevskaya*, 1, Aida G Gabdoulkhakova1, Julia V Filina1, Aleksey I Zabotin2, Anatoly P Tsibulkin1
Identifiers and Pagination:Year: 2011
First Page: 36
Last Page: 44
Publisher ID: TORJ-5-36
Article History:Received Date: 30/6/2011
Revision Received Date: 30/7/2011
Acceptance Date: 3/8/2011
Electronic publication date: 18/10/2011
Collection year: 2011
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
The aim of this work was to study the peripheral blood monocyte functions in patients with advanced RA and their predisposed to RA relatives in comparison with those in women, not hereditary tainted with autoimmune diseases (donors). In groups comprising 24 RA patients, 24 relatives, and 24 donors the following monocyte functions were assessed: engulfment and digestion (radioisotope method); release of lysosomal glucuronidase in response to opsonized zymosan (fluorescent method); reactive oxygen species (ROS) generation (chemiluminescence), and serum levels of proinflammatory cytokines (ELISA). The monocyte specific feature in patients and their relatives is chiefly extracellular digestion due to the delayed engulfment. The digestive activity, probably inhibited in relatives, is increased in advanced RA. ROS generation by the cells and serum levels of TNF-alpha and IL-1-beta are abundant both in the patients and their relatives.
High levels of pro-inflammatory cytokines, presumably, of monocyte origin, and increased levels of stimulated ROS generation may be due to the priming and prolonged activation of monocytes in relatives.
We show for the first time that the functioning of circulating mononuclear phagocytes in the assumed to be healthy predisposed to RA individuals differs from that in the healthy people not hereditary tainted with autoimmune diseases and in general resembles the functioning of the cells in the patients with advanced RA.