1,721,247 research outputs found
Anticitrullinated protein/peptide antibodies and rheumatoid factors: two distinct autoantibody systems
No full textIn a previous issue of Arthritis Research and Therapy, Ursum and colleagues report the relative stabilities of anticitrullinated protein/peptide antibodies (ACPAs) and IgM rheumatoid factors during the course of rheumatoid arthritis and their differential correlation with markers of the acute-phase response. These findings add to a growing body of evidence highlighting the distinct nature of these two autoantibody systems and the role of ACPAs as a disease-specific marker of rheumatoid arthritis
New facet of antiphospholipid antibodies
No full textSince the aCL test was first described, several reports have described the heterogeneity of aPL, which binds to different anionic phospholipids, proteins, or to a phospholipid–protein complex. It has been recently reported that antiphospholipids (aPLs) from the sera of patients with the antiphospholipid syndrome (APS) are able to bind some newly identified antigens, the lyso(bis)phosphatidic acid (LBPA), lipid restricted to the late endosomes, and the sulfatides, acidic glycosphingolipids involved in the hemostatic process. Of interest, aLBPAs are present in the sera of a large number of patients with APS showing similar sensitivity and specificity compared to anti- 2 glycoprotein I antibodies (a2 -GPIs) and close association with lupus anticoagulant. Moreover, 2 -GPI binds to sulfatides and the majority of the aPL reacting with cardiolipin–2 -GPI complex also react with the sulfatide–2 -GPI complex. Different mechanisms involved in the production of autoantibodies in autoimmune diseases have been proposed and, among them, apoptosis or programmed cell death seems to play a leading role. The relocation of CL and its metabolites during apoptosis may represent an in vivo trigger for the generation of aCL, and the higher reactivity of sera from APS patients to monolysocardiolipin, the immediate degradation product of mitochondrial CL validates this hypothesis. Finally, increasing evidence suggests that oxidative stress could be a pathogenic link between aPL and thrombosis, and antioxidant treatment may have some efficacy in preventing the clinical manifestations of this syndrome
Role of anti-glial fibrillary acidic protein antibodies in the pathogenesis of neuropsychiatric systemic lupus erythematosus should be clarified: comment on the article by Trysberg et al
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Determinazione degli anticorpi anti-peptide citrullinato nel liquido sinoviale di pazienti con artrite reumatoide
No full textThe role of anti-cyclic cytrullinate antibodies testing in rheumatoid arthritis
No full textRheumatoid arthritis (RA) is a chronic, progressive inflammatory disease, which leads to joint destruction and deformity and is often accompanied by systemic complications. It is generally considered an autoimmune disease characterized by several autoantibodies. The impressive advances made in understanding the biological mechanisms of RA have led to more focused, directed therapies that have joined, and in many cases overcome, more traditional treatments. Along the last decade, the so-called biological anti-TNF-alpha agents have been shown to reduce disease activity, to slow disease progression and to improve patients' quality of life. The clear evidence that an early therapeutic intervention improves the overall outcome of the disease supports the importance of an early diagnosis. In the last years, several studies showed that anti-cyclic citrullinated peptide antibodies (anti-CCP) represent a sensitive and specific serologic marker for RA. Moreover, a large body of evidence has shown that anti-CCP may also serve as an early diagnostic and prognostic marker in RA. The aim of this article is to provide an overview of the current state of knowledge regarding anti-CCP focusing in particular on their clinical specificity and prognostic value in RA. © 2007 Humana Press Inc
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