1990
DOI: 10.1038/icb.1990.4
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Antibodies to type II collagen in SLE: A role in the pathogenesis of deforming arthritis?

Abstract: Summary The role of autoimmunity to type II collagen in the arthritis of systemic lupus erythematosus (SLE) has been assessed by ELISA and by Western blotting cyanogen bromide cleavage fragments separated on SDS-PAGE. The results show that antibodies to both native and heat-denatured collagen are quite common in SLE when measured by ELISA. Of particular interest is the demonstration of an association between antibodies to the CB 11 peptide and deforming arthritis in SLE. This is the arthritogenic peptide in mu… Show more

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Cited by 15 publications
(7 citation statements)
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“…Serum autoantibodies against native and denatured type II collagen (anti-NCII and DCII) are detected in 24–30% of patients with RA, as shown by cross-sectional studies on patients with well-established disease [5-8]. However, this relatively low frequency in RA of anti-CII, together with seropositivity (albeit at even lower frequency) in other rheumatological and inflammatory diseases [7] including psoriatic arthritis (PsA) [7,9], osteoarthritis (OA) [7,10,11], juvenile arthritis [12], Paget's disease [10,11], and systemic lupus erythematosus [6,7,10,13], has negated the diagnostic utility and pathogenetic significance of anti-CII in RA. However, several studies have reported that the frequency of anti-NCII might be as high as 60–75% in patients with RA when tested very early in the disease [14-16], and thereafter frequencies tend to fall to those ascertained in the earlier cross-sectional studies [17], suggesting that their presence might provide a sensitive predictive marker for cases of early RA.…”
Section: Introductionmentioning
confidence: 99%
“…Serum autoantibodies against native and denatured type II collagen (anti-NCII and DCII) are detected in 24–30% of patients with RA, as shown by cross-sectional studies on patients with well-established disease [5-8]. However, this relatively low frequency in RA of anti-CII, together with seropositivity (albeit at even lower frequency) in other rheumatological and inflammatory diseases [7] including psoriatic arthritis (PsA) [7,9], osteoarthritis (OA) [7,10,11], juvenile arthritis [12], Paget's disease [10,11], and systemic lupus erythematosus [6,7,10,13], has negated the diagnostic utility and pathogenetic significance of anti-CII in RA. However, several studies have reported that the frequency of anti-NCII might be as high as 60–75% in patients with RA when tested very early in the disease [14-16], and thereafter frequencies tend to fall to those ascertained in the earlier cross-sectional studies [17], suggesting that their presence might provide a sensitive predictive marker for cases of early RA.…”
Section: Introductionmentioning
confidence: 99%
“…In view of this, as with lupus nephritis classification, we should adequately classify LA earlier to identify patients who have a more aggressive phenotype that resembles RA patients. The utilization of serological markers [17][18][19] and the use of joint US or MRI to identify patients with LA at risk of developing deforming arthritis are promising, but, until now, they are of little practical use and of low accessibility in the rheumatologist's office routine.…”
Section: Discussionmentioning
confidence: 99%
“…Several previous studies have attempted to associate JA with the presence of autoantibodies, such as anti-dsDNA, ACL, and type II anticollagen, but they showed conflicting results 21–23 . One study observed that the serum of patients with SLE and JA presents with higher levels of interleukin 6 (IL-6) than in those with SLE, but without JA 24 .…”
Section: Discussionmentioning
confidence: 99%
“…Several previous studies have attempted to associate JA with the presence of autoantibodies, such as anti-dsDNA, ACL, and type II anticollagen, but they showed conflicting results. [21][22][23] One study observed that the serum of patients with SLE and JA presents with higher levels of interleukin 6 (IL-6) than in those with SLE, but without JA. 24 Although it lacks sufficient specificity to be considered a biomarker for JA in SLE, increased IL-6 in this clinical setting may suggest that the use of biological molecules, such as tocilizumab (anti-IL-6), may have a place in the treatment of SLE and perhaps prevent the development of JA.…”
Section: Discussionmentioning
confidence: 99%