Study Finds Inflammation Mechanisms In Rheumatoid Arthritis Patients

Study Finds Inflammation Mechanisms In Rheumatoid Arthritis Patients

In a newly published paper in Mediators of Inflammation journal entitled “Differences of IL-1β Receptors Expression by Immunocompetent Cells Subsets in Rheumatoid Arthritis“, scientists reported new insights into the mechanisms of the inflammation process occurring in rheumatoid arthritis (RA) patients, as they investigated the expression of IL-1β-membrane-bound receptors before and after a course of basic therapy.

Rheumatoid arthritis is an autoimmune disorder characterized by inflammation of the connective tissue mostly accompanied by lesions, erosion and degenerative changes in joints. Patients with RA mostly experience painful joints and other symptoms like fever, fatigue, low red blood cells and inflammation around the lungs/heart. Unfortunately, there is no cure for RA, but the disease could be managed by medications, surgery, regular exercise, dietary supplements, vaccination, and alternative medicines. In the US, between 200,000 to 3 million individuals reportedly live with RA and the disease results in about 50,000 deaths per year worldwide.

Although the causes and mechanisms of RA are still not fully understood, it is believed that the illness is mainly induced by an autoimmune process of the body. Recent studies suggested that broad range of cells like various white blood cells (monocyte, T cells, B cells) are involved in the pathogenesis of RA. Also, a protein named interleukin-1β (IL-1β) believed to mediate intercellular communication, is involved in RA development, and increased production of this protein causes destruction of the bone tissue. On the other hand, it was suggested that IL-1β activity is induced and regulated by soluble and membrane-bound receptors, and its effectiveness depends not only on the percentage of receptor-positive cells but also on the density of expressed receptors.

In this study, the team investigated expression of IL-1β-membrane-bound receptors in RA patients before and after therapy in comparison with healthy controls. Blood samples were collected from each patient during the acute stage of the disease and after effective course of treatment with methotrexate therapy, Rituximab or methylprednisolone. Afterwards, the samples were analyzed by standard biochemical methods to determine IL-1β protein levels in blood serum.

The results suggested differences in the levels of expressed IL-1β receptors among white blood cells (T cells, B cells, monocytes) between patients with RA and healthy controls. Specifically, white blood cells (B cells and monocytes) showed opposite changes in percentage of receptor-positive cells and the number of receptors between RA patients and healthy controls.

“The resulting data are indicative of differences in expression of IL-1β receptors in various subpopulations of immunocompetent cells in normal cells and in pathology. Additionally, they show changes both in indicators of mediator production accompanying inflammatory pathologies and in the system of receptor regulation on the cell surface. Therefore, it is important to determine both the relative percentage of cells expressing receptors to immunomodulatory cytokines and the levels of membrane-bound receptors, because the density of expression is characterized by disease-induced changes that cannot be detected when assessing the percentage of positive cells,” the authors conclude in their study.

These novel data show that the correlations between parameters of soluble mediators in RA patients who respond to treatment and those in the same patients in the acute phase can be used to attest treatment effectiveness.

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