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Anti Ccp Quest
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Collagen autoantibody and its relationship with CCP antibody and rheumatoid factor in the progression of early rheumatoid arthritis
Date received: 10 November 2016 / Date revised: 28 February 2017 / Date accepted: 6 March 2017 / Date published: 5 April 2017
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Serum autoantibodies cyclic citrullinated peptide (anti-CCP) and rheumatoid factor (RF) are important diagnostic and prognostic markers in rheumatoid arthritis (RA), but their autoantigens are not specific for cartilage. Antibodies specific to type II collagen (CII) also occur in RA, and similar monoclonal antibodies can cause collagen-induced arthritis in animals, but their role in RA is uncertain. We used enzyme-linked immunosorbent assay (ELISA) and CII's CB10 peptide to compare the frequency of autoantibodies and anti-CCP and RF in stored sera from a prospective study of 82 early-stage RA patients to assess the results, explains. Such as remission (n = 23), chronic arthritis (n = 27) or erosion (n = 32). The initial frequencies of anti-CB10, anti-CCP, and RF were 76%, 54%, and 57% in RA, and 4%, 0%, and 9% in controls, respectively. The frequency of anti-CB10 was not associated with outcome, but anti-CCP and RF increased with severity, and the number of autoantibodies reflected severity. We propose that RA is an immune complex-mediated arthritis in which three antibodies interact and anti-CII causes local cartilage damage and inflammation, leading to citrullination of articular proteins, neo-epitope formation, and strong CCP responses. In genetically susceptible subjects, all of these are amplified and modified by radiofrequency.
Rheumatoid arthritis is a chronic inflammatory arthritis of unknown cause. Back in the late 1940s, when rheumatoid factor (RF) was first identified in patients with rheumatoid arthritis, some evidence suggested that the culprit was autoimmune. However, accurate early diagnosis is difficult, and clinical diagnosis is based on the exclusion of other possible diseases by rheumatologists, and consideration of whether they meet the criteria proposed by the American Rheumatology Association (ARA) in 1954 and revised in the following years [1, 2, 2] 3, 4]. These approaches define the disease more precisely and have attracted extensive research into the clinical, histological, immunological, pharmacological, and genetic aspects of RA and resolved controversial issues about understanding the disease. These findings largely confirm the hypothesis that the underlying mechanisms of RA are independent, but have not confirmed the identity of joint-specific autoantigens involved in immune tolerance failure.
RF as a diagnostic hallmark of RA may precede clinical symptoms by many years [5] and is associated with severe disease and poor prognosis. Evidence for intra-articular accumulation of RF, its presence in immune complexes with IgG, and low levels of complement in synovial fluid and cartilage suggest that immune complexes may be an important component of impaired inflammation [6, 7, 8, 9, 10, 11]. However, the relationship between RF and RA remains unclear. The finding of low titers of RA in chronic infection, healthy subjects after vaccination, and in primary Sjogren's syndrome and other connective tissue diseases without arthritis is not specific [12, 13, 14]. In addition, its epitope is the Fc region of immunoglobulin G (IgG), which is not part of the joint structure.
Antibodies to citrullinated protein (ACPA), commonly expressed as cyclic citrullinated peptide antibodies (anti-CCP), have been identified as the major autoantibodies in RA and appear to be particularly associated with arthritis [15]. Citrulline is obtained by the removal of arginine by peptidylarginine deiminase (PADI) found in macrophages and neutrophils [16]. An anti-CCP assay has been developed that can detect the activity of ACPA by a series of citrullinated proteins [17]. Known protein antigens have rarely been identified and vary in specificity and affinity between individuals, but the activity of ACPA with citrullinated fibrinogen, alpha enolase, vimentin, and collagen type II (CII) is the most commonly studied [18, 19, 20]. Like RF, ACPA precedes the clinical manifestations of RA [21, 22, 23], is produced intra-articularly [24, 25], and is present in high titers in severe arthritis [26]. When first reported, ACPA and anti-CCP appeared to be somewhat specific for RA, but antibodies have recently been identified in other diseases [27, 28, 29]. ACPA responses are largely dependent on alleles of the histocompatibility leukocyte antigen (HLA)-DRB1 representing a shared epitope associated with RA (SE) [30]. SE binds strongly to citrulline for T cell presentation [31], and ACPA production is thought to be in response to neo-epitopes due to citrullination.
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Although RF and most known anti-citrullinated protein antigens are not restricted to joints, one possible autoantigen is type II collagen, which was first proposed by Steffen in 1970 as an autoantigen in RA [32]. Antibodies to CII are recurrently present in serum and synovial fluid, especially at the onset of the disease, although serum antibody levels may decrease as the disease progresses [33, 34, 35]. Anti-CII is synthesized within the synovium [36], and collagen-containing immune complexes have been described in synovial fluid [9, 37, 38]. In animals, CII is arthritic, and injection of native CII in adjuvant induces collagen-induced arthritis (CIA), characterized by antibodies against CII and inflammatory polyarthritis [39, 40]. Variability in arthritic manifestations is associated with the expression of certain alleles of the major histocompatibility complex (MHC) class II [41] and depends on a robust immune system: lack of B cells [42] or lack of compatibility [43] were protected. Furthermore, a monoclonal antibody (mAb) against CII found in mice with CIA could induce collagen antibody-induced arthritis (CAIA) in naive mice. CAIA is characterized by inflammation, pannus formation, and bone erosion similar to that seen in RA [44]. This disease model does not require the help of T cells and is an instructive model of how the immune system causes arthritis. Rheumatoid arthritis is not restricted to MHC and can be induced in many mouse strains, representing a valid CIA-arm model, but depending on the specificity of the antibody used. These arthritic mAbs recognize epitopes in CII that share a common amino acid motif, the arginine-glycine-hydrophobic acid triplet, and map to surface-exposed regions of collagen fibrils accessible to antibody binding [44]. The epitope is conserved and recognized by antibodies from mouse [45, 46, 47, 48] and human RA [36, 46]. Interestingly, large arthritic epitopes on collagen fibrils containing exposed arginines can also be citrullinated [49], and monoclonal antibodies directed against these citrullinated epitopes may themselves cause arthritis , or cause arthritis. The joints deteriorated when small doses of anti-CII were injected [50].
Taken together, these studies suggest that all three classes of autoantibodies may play a role in the development and progression of RA. However, while several studies have used measurements of serum RF or anti-CCP to investigate the impact of early RA, none of these studies included anti-CII because there is no standard anti-CII test yet. usable. We previously detected CII antibodies using an ELISA in which the intact CII molecule was replaced by a helical CB10 fragment of the native CII molecule [51]. CB10, one of two major peptides found upon digestion of CII with cyanogen bromide, contains an important arthritic epitope in animal studies and accounts for 30% of intact CII. Using this CB10 ELISA, we detected autoantibodies in 84 (88%) of 96 RA patients compared to 24% using unmodified CII. In contrast, anti-CB10 was present in only 4 of 33 patients (12%)
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