OBJECTIVE: To investigate the occurrence of anti-annexin V autoantibodies in sera of patients with rheumatoid arthritis to assess involvement with the disease and any relation to glucocorticoid treatment. METHODS: Anti-annexin V antibodies were measured by an enzyme linked immunosorbent assay (ELISA) which used the purified human recombinant protein as antigen. RESULTS: Concentrations of anti-annexin V autoantibodies, predominantly of the IgG class, were significantly raised in sera from patients with rheumatoid arthritis compared to normal controls. This was not correlated with other indices of disease activity such as erythrocyte sedimentation rate or C reactive protein and was unrelated to glucocorticoid treatment. CONCLUSIONS: Extracellular annexin V provides an antigenic stimulus for autoantibody production and its in vivo expression is independent of glucocorticoid control. Such autoantibodies may have a detrimental role in the arthritic condition by interfering with putative functions of annexin V, including collagen type II binding, inhibition of phospholipase A2 activity, and Fc receptor activity.
OBJECTIVE: To investigate the occurrence of anti-annexin V autoantibodies in sera of patients with rheumatoid arthritis to assess involvement with the disease and any relation to glucocorticoid treatment. METHODS: Anti-annexin V antibodies were measured by an enzyme linked immunosorbent assay (ELISA) which used the purified human recombinant protein as antigen. RESULTS: Concentrations of anti-annexin V autoantibodies, predominantly of the IgG class, were significantly raised in sera from patients with rheumatoid arthritis compared to normal controls. This was not correlated with other indices of disease activity such as erythrocyte sedimentation rate or C reactive protein and was unrelated to glucocorticoid treatment. CONCLUSIONS: Extracellular annexin V provides an antigenic stimulus for autoantibody production and its in vivo expression is independent of glucocorticoid control. Such autoantibodies may have a detrimental role in the arthritic condition by interfering with putative functions of annexin V, including collagen type II binding, inhibition of phospholipase A2 activity, and Fc receptor activity.
Authors: N J Goulding; M R Podgorski; N D Hall; R J Flower; J L Browning; R B Pepinsky; P J Maddison Journal: Ann Rheum Dis Date: 1989-10 Impact factor: 19.103
Authors: K F Chung; M R Podgorski; N J Goulding; J L Godolphin; P R Sharland; B O'Connor; R J Flower; P J Barnes Journal: Respir Med Date: 1991-03 Impact factor: 3.415
Authors: F C Arnett; S M Edworthy; D A Bloch; D J McShane; J F Fries; N S Cooper; L A Healey; S R Kaplan; M H Liang; H S Luthra Journal: Arthritis Rheum Date: 1988-03
Authors: J K Rivers; M R Podgorski; N J Goulding; E Wong; J A McGrath; R J Flower; M W Greaves Journal: Br J Dermatol Date: 1990-11 Impact factor: 9.302
Authors: Christophe M M Lahorte; Jean-Luc Vanderheyden; Neil Steinmetz; Christophe Van de Wiele; Rudi A Dierckx; Guido Slegers Journal: Eur J Nucl Med Mol Imaging Date: 2004-05-12 Impact factor: 9.236
Authors: Leigh G Griffiths; Leila H Choe; Kenneth F Reardon; Steven W Dow; E Christopher Orton Journal: Biomaterials Date: 2008-06-02 Impact factor: 12.479
Authors: Lawrence L Horstman; Wenche Jy; Carlos J Bidot; Yeon S Ahn; Roger E Kelley; Robert Zivadinov; Amir H Maghzi; Masoud Etemadifar; Seyed Ali Mousavi; Alireza Minagar Journal: J Neuroinflammation Date: 2009-01-20 Impact factor: 8.322