Anticentromere Autoantibodies in Patients without Raynaud's Disease or Systemic Sclerosis

Vázquez‐Abad, Dolores; Grodzicky, Tamara; Senécal, Jean‐Luc

doi:10.1006/clim.1998.4643

Cited by 7 publications

(1 citation statement)

References 18 publications

(27 reference statements)

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“…Since these initial studies, the clinical associations of anti-CENP have widened. One recent study confirmed the disease specificity of anti-CENP antibodies while two other studies using different technologies including different LIA and addressable laser bead assays (ALBIA) have reported ACA in other systemic rheumatic diseases such as SLE (1.8 -5.6%) or RA (2.2%) [118][119][120][121][122][123][124][125][126][127][128][129][130][131]. The anti-CENP reactivity in RA patients might be attributed to cross-reactive antibodies that react with both CENP-B and heterogeneous nuclear RNP (hnRNP) [132] or to the CENP-A epitope motif G/A-P-R/S-R-R (reviewed in [133,[134][135][136]).…”

Section: Anti-cenpmentioning

confidence: 95%

Challenges and Controversies in Autoantibodies Associated with Systemic Rheumatic Diseases

Mähler¹,

Raijmakers²,

Fritzler

2007

CRR

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Since the first identification of self-reactive antibodies in systemic lupus erythematosus and other systemic autoimmune rheumatic diseases, many autoantibodies have been identified as useful probes in molecular and cell biology and as diagnostic and prognostic biomarkers in clinical immunology. Among the autoantigens, double-stranded desoxoribonucleic acid (dsDNA), the Smith antigen (Sm), ribonucleoproteins (RNP), Scl-70 (topoisomerase I), proliferating cell nuclear antigen (PCNA), and others were described as serologic hallmarks in the diagnosis of systemic autoimmune rheumatic diseases. Despite these advances in identifying autoantibody markers, a number of challenges and controversies persist concerning their origin, clinical usefulness and relevance. These include the association between anti-ribosomal P antibodies and clinical features in systemic lupus erythematosus, the disease specificity of several autoantibodies (i.e. chromatin, Jo-1, alpha-fodrin, topo I and CENP), the relationship between the SS-A/Ro52 and SS-A/Ro60 autoantibody system(s) and the detection of anti-RNP/Sm and anti-fibrillarin antibodies.

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Section: Anti-cenpmentioning

confidence: 95%

Challenges and Controversies in Autoantibodies Associated with Systemic Rheumatic Diseases

Mähler¹,

Raijmakers²,

Fritzler

2007

CRR

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Incidence and clinical correlation of anticentromere antibody in Thai patients

et al. 2005

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Anticentromere antibodies (ACA) are useful in assessing and classifying patients with mild variant of systemic sclerosis called calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias (CREST) syndrome. From their prognostic significance, we are interested in the prevalence and disease correlation in Thai patients. A total of 3,233 serum samples of patients with any musculoskeletal symptoms were sent for antinuclear antibody determination at Ramathibodi Immunology Laboratory Service between the years 1998 and 2001. Forty sera (1.23%) were ACA positive. These sera were from 27 patients with autoimmune diseases and 13 with nonautoimmune diseases. Among autoimmune group, scleroderma was the most common diagnosis (33.3%) with limited sclerosis being the most frequent variant. The percentages of autoimmune disease were almost the same among the low-titer (1:40) and the high-titer (1:640) groups. The study suggests that the prevalence of ACA in Thai patients is low. The presence of ACA detected in patients with vague musculoskeletal symptoms does not suggest a diagnosis of CREST syndrome. Even high-titer ACA can be found in nonautoimmune diseases.

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Anti-CENP-B and anti-TOPO-1-containing sera from systemic sclerosis-related diseases with Raynaud’s phenomenon induce vascular endothelial cell senescence not via classical p53-p21 pathway

Shen

Lai

et al. 2017

Clin Rheumatol

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Raynaud's phenomenon (RP) is the earliest and most common clinical manifestation in patients with systemic sclerosis (SSc) and its related diseases containing anti-TOPO-1 and/or anti-CENP-B autoantibodies in the sera. However, the cause-effect relationship between the two autoantibodies and RP remains elucidation. Sera containing anti-CENP-B and anti-TOPO-1 autoantibodies were obtained from SSc-related diseases manifesting RP. The polyclonal auto-antibodies were purified from pooled sera by affinity chromatography. Mouse monoclonal anti-CENP-B and anti-TOPO-1 were purchased. Calf pulmonary arterial endothelial cells (CPAE) were incubated with 40% patient sera, purified polyclonal antibodies or mouse monoclonal antibodies for 1-6 days. The vascular endothelial biomarkers von Willebrand factor (vWF), thrombomodulin (CD141) and 6-keto-prostaglandin F1α (6-keto-PGF1α), cell viability marker ATP, and cell necrosis/lysis marker LDH in the culture supernatants were measured by ELISA. The cell senescence biomarker β-galactosidase and telomere content in the cells were stained by the respective kit. The classical p53-p21 senescence pathway was detected by Western blot. We found that 40% anti-CENP-B or anti-TOPO-1-containing sera without heat-inactivation and mouse monoclonal antibodies suppressed 6-keto-PGF1α production, increased β-galactosidase, and decreased relative telomere content. The cell senescence effects were proved not via p53-p21 pathway. The pathognomonic anti-CENP-B and anti-TOPO-1 autoantibodies in SSc-related diseases accelerate vascular endothelial cell senescence and functional impairment inducing RP. The real signaling pathway for autoantibody-induced cell senescence remains exploration.

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Anticentromere Autoantibodies in Patients without Raynaud's Disease or Systemic Sclerosis

Cited by 7 publications

References 18 publications

Challenges and Controversies in Autoantibodies Associated with Systemic Rheumatic Diseases

Challenges and Controversies in Autoantibodies Associated with Systemic Rheumatic Diseases

Incidence and clinical correlation of anticentromere antibody in Thai patients

Anti-CENP-B and anti-TOPO-1-containing sera from systemic sclerosis-related diseases with Raynaud’s phenomenon induce vascular endothelial cell senescence not via classical p53-p21 pathway

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