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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 primary rheumatoid arthritis.
Date received: 10 November 2016 / Date revised: 28 February 2017 / Date accepted: 6 March 2017 / Date published: 5 April 2017
Identification Of Autoantibodies Against Transthyretin For The Screening And Diagnosis Of Rheumatoid Arthritis
Serum autoantibodies cyclic citrullinated peptide (anti-CCP) and rheumatoid factor (RF) are important signs and symptoms in rheumatoid arthritis (RA), but their autoantigens are not cartilage-specific. Autoantibodies to tissue-specific collagen type II (CII) also occur in RA, and monoclonal antibodies with specific antigens drive the disease. the collagen antibody-induced in animals, but their role in RA is not certain. We used enzyme-linked immunosorbent assay (ELISA) with CII's CB10 peptide to compare the abundance of autoantibodies with anti-CCP and RF in sera collected from a prospective study of 82 early RA patients to investigate results, defined as remission (n = 23), non-destructive arthritis (n = 27) or erosion (n = 32). First-line anti-CB10, anti-CCP and RF were 76%, 54% and 57% in RA and 4%, 0% and 9% in 136 controls, respectively. The time of anti-CB10 was not related to the results, but the anti-CCP and RF increased in strength, and the number of autoantibodies reflects the weight. We suggest that RA is a complex inflammatory disease in which three diseases interact and that anti-CII induces local cartilage damage and inflammation, leading to protein citrullination adhesion, formation of neoepitopes, and the dynamic response of the subjects involved. , both amplified and modified by RF.
Rheumatoid arthritis is an inflammatory arthritis of unknown etiology. Back in the late 1940s, when rheumatoid factor (RF) was first found in patients with rheumatoid arthritis, clinical evidence suggested that the culprit was autoimmune. However, early accurate diagnosis is difficult and specific tests are performed by rheumatologists after excluding other relevant tests and considering the criteria established by the American Rheumatology Association (ARA) in 1954 and again reviewed in later years [1, 2, 3, 4]. These principles accurately define the disease and have attracted extensive research in the clinical, histological, immunological, pharmacological, and genetic fields. -treatment of RA and resolve conflicting issues regarding understanding of the disease. These studies strongly support the idea that the basis of RA is autoimmunity, but the definition of specific autoantigens involved in immune tolerance remains unclear.
RF is a prognostic indicator for RA that may precede clinical symptoms by many years [5] and is associated with more severe disease and poor prognosis. The evidence for the use of RF, its presence in complex complexes with IgG, and low concentration in synovial fluid and cartilage suggest that immune complexes can be and areas of severe inflammation [6, 7, 8, 9, 10, 11] . However, the relationship between RF and RA remains unclear. A low number of RA is found in infectious diseases, health issues after vaccination, and Sjogren's syndrome and other related diseases without non-specific disease [12, 13, 14]. In addition, its epitope is the Fc part of immunoglobulin G (IgG), which is not a structural part of the joint.
Antibodies to citrullinated protein (ACPA), often expressed as cyclic citrullinated peptide antibodies (anti-CCP), have been identified as the main autoantibodies in RA and seem to be particularly associated with erosive disease [15]. Citrulline is obtained from the deimination of arginine by peptidyl-arginine-deiminase (PADI) found in macrophages and neutrophils [16]. Anti-CCP tests have been developed to detect ACPA reactive with many citrullinated proteins [17]. Putative protein antigens are rare and vary in specificity and affinity between individuals, but ACPA reactive and citrullinated fibrinogen, alpha enolase, vimentin, and collagen type II (CII) are the most common. then studied frequently [18, 19, 20]. Like RF, ACPA is produced intra-articularly [24, 25] before the onset of disease in RA [21, 22, 23], and it occurs at a high Titers present [26]. When first reported, ACPA and anti-CCP appeared to be specific for RA, but antibodies have recently been identified in other diseases [27, 28, 29]. ACPA responses are largely dependent on histocompatibility leukocyte antigen (HLA)-DRB1 antigens representing shared epitopes (SE) [30]. SE binds strongly to citrulline for T cell presentation [31], and ACPA production is thought to respond to neo-epitopes that produce citrullination.
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Although RF and many anti-citrullinated protein antigens are not limited to joints, one specific autoantigen is type II collagen, which was first proposed by Steffen in 1970 as an autoantigen for RA [32]. Antibodies to CII persist in serum and synovial fluid, especially at the beginning of the disease, although serum antibody levels may decrease as the disease progresses [ 33 , 34 , 35 ]. Anti-CII is synthesized in the joints [36], and it is present in the collagen protective complex in the synovial fluid that has been described [9, 37, 38]. In animals, CII is fat, and injection of real CII in the aid induces collagen-induced arthritis (CIA), characterized by antibodies against CII and inflammatory polyarthritis [39 , 40]. The variability of the expression of the tumor is related to the expression of the class II major histocompatibility (MHC) alleles [41] and it depends on the immune system: B cell deficient [42] or incomplete attachment [ 43] protected animals. In addition, the monoclonal antibody (mAb) against CII from CIA mice can induce collagen antibody-mediated disease (CAIA) in naive mice. CAIA is characterized by inflammation, formation of pannus, and bone erosion, which is similar to what has been observed in RA [44]. This disease model does not require the help of T cells and is an example of how antibodies can cause arthritis. The disease is not MHC restricted and can be induced in many mouse diseases, representing an example of a dynamic arm. of CIA, but depends on the specificity of the antibody used. These arthritic mAbs recognize epitopes on CII that share a common amino acid sequence, the arginine-glycine-hydrophobic acid triplet, and map on the collagen fibrils available for antibody binding to the exposed part [44]. These epitopes are conserved and are also recognized by antibodies from mice [45, 46, 47, 48] and humans with RA [36, 46]. Interestingly, many antigens on collagen fibers containing arginine exposed on the surface can also be neutralized [49], and mAbs react to these citrullinated epitopes can cause illness, or induce more illness when injected with specific doses of anti-CII. 50].
Together, these studies suggest that all three autoantibodies may play a role in the development and progression of RA. However, although many studies have used serum RF or anti-CCP levels to assess outcomes in early RA, none of these studies included anti-CII because no standard clinical studies for anti-CII are currently available. We first used an ELISA, in which the CII molecule is replaced by the three-helical CB10 region of the real CII molecule, to detect CII antibodies [51]. CB10, one of the two major peptides derived from the oxidation of CII and cyanogen bromide, has an important fat epitope in animal studies, accounting for 30% of the total CII. Using this CB10 ELISA, we found autoantibodies in 84 (88%) of 96 RA patients compared to only 24% using the full CII. In contrast, only 4 of 33 (12%) patients received anti-CB10
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