Review Article - Rheumatoid Arthritis & Il-6
Review Article
RA: Interleukin-6, its roles and significance in the pathophysiology of Rheumatoid Arthritis
Introduction
Rheumatoid arthritis (RA) is an inflammatory autoimmune condition principally causing synovial joint inflammation and cartilage erosion. The pathogenesis encompasses intricate cellular and humoural manifestations, and vascular reactions that result in the infiltration of the synovium by white blood cells, of which release inflammatory mediators, inclusive of Interleukin-6 (IL-6). IL-6 serum levels of RA patients as shown by Capell et al. (1993) displayed a median of 55 IU/ml, as compared to that of healthy controls of 10 IU/ml. With a wide-ranging pleiotropy endorsed by both a membrane-bound (IL-6R) and soluble (sIL-6R) receptor, and by the relative omnipresence of the trans-membrane protein gp130, IL-6 endorses a pro-inflammatory effect via its influence on numerous cell types and signalling-pathways. As a result, heightened levels of IL-6 aids in the promotion of osteitis, sequential joint damage, pain/discomfort and impaired function in RA patients.
Pleiotropy of IL-6
Interleukin 6 exerts effects on numerous pathways contributing to the pathophysiology of RA. IL-6 as it is called today has been known by several names that exemplify its pleiotropy for example, hepatocyte-stimulating factor known to cause the induction of C-reactive protein (CRP); due to IL-6 association with synovial fibril aggregation has been known as Amyloid protein; a thrombopoietin; both B-cell differentiation and stimulating factor 2; plasmacytoma growth factor; and cytotoxic T-cell differentiation factor. It also causes the differentiation of Th17 cells; is a causative factor in adhesion molecule expression on the surface of endothelial cells, and is involved in the differentiation to mature from precursor osteoclasts cells (REF!!).
IL-6
Recptor binding
IL-6 implements its influence via a protein complex primarily comprised of a membrane bound IL-6R and
RA: Interleukin-6, its roles and significance in the pathophysiology of Rheumatoid Arthritis
Introduction
Rheumatoid arthritis (RA) is an inflammatory autoimmune condition principally causing synovial joint inflammation and cartilage erosion. The pathogenesis encompasses intricate cellular and humoural manifestations, and vascular reactions that result in the infiltration of the synovium by white blood cells, of which release inflammatory mediators, inclusive of Interleukin-6 (IL-6). IL-6 serum levels of RA patients as shown by Capell et al. (1993) displayed a median of 55 IU/ml, as compared to that of healthy controls of 10 IU/ml. With a wide-ranging pleiotropy endorsed by both a membrane-bound (IL-6R) and soluble (sIL-6R) receptor, and by the relative omnipresence of the trans-membrane protein gp130, IL-6 endorses a pro-inflammatory effect via its influence on numerous cell types and signalling-pathways. As a result, heightened levels of IL-6 aids in the promotion of osteitis, sequential joint damage, pain/discomfort and impaired function in RA patients.
Pleiotropy of IL-6
Interleukin 6 exerts effects on numerous pathways contributing to the pathophysiology of RA. IL-6 as it is called today has been known by several names that exemplify its pleiotropy for example, hepatocyte-stimulating factor known to cause the induction of C-reactive protein (CRP); due to IL-6 association with synovial fibril aggregation has been known as Amyloid protein; a thrombopoietin; both B-cell differentiation and stimulating factor 2; plasmacytoma growth factor; and cytotoxic T-cell differentiation factor. It also causes the differentiation of Th17 cells; is a causative factor in adhesion molecule expression on the surface of endothelial cells, and is involved in the differentiation to mature from precursor osteoclasts cells (REF!!).
IL-6
Recptor binding
IL-6 implements its influence via a protein complex primarily comprised of a membrane bound IL-6R and
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