Human anticentriole autoantibody in patients with scleroderma and Raynaud's phenomenon

Möroi, Y; Murata, Ichirô; Takeuchi, Akiteru; Kamatani, Naoyuki; Tanimoto, Kiyoaki; Yokohari, R

doi:10.1016/0090-1229(83)90041-7

Cited by 39 publications

(21 citation statements)

References 12 publications

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“…Anti-centriole antibodies are seen in association with primary Raynaud's phenomenon and scleroderma [131,132]. Anti-p80-coilin antibodies have been isolated from the sera of five patients from a serum bank of 810 Japanese patients with 'collagen diseases'.…”

Section: Other Autoantibodiesmentioning

confidence: 99%

Untitled

Reveille

2003

Arthritis Res Ther

183

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80ACA = anti-centromere antibodies; aCL = anticardiolipin antibodies; AFA = antifibrillarin/anti-U3-RNP; ANA = anti-nuclear antibodies; ANCA = anti-neutrophil cytoplasmic antibodies; ANoA = anti-nucleolar antibodies; anti-RNAP = anti-RNA-polymerase antibodies; anti-Sm = anti-Smith antibodies; aPL = antiphospholipid antibodies; β 2 gp I = β 2 glycoprotein I antibodies; CENP = centromeric nucleoprotein; CIE = counterimmunoelectrophoresis; CREST = a variant of SSc defined by the presence of calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangectasia; CTD = connective tissue diseases; dcSSc = diffuse cutaneous systemic sclerosis; DL CO = diffusion capacity for carbon monoxide; DM = dermatomyositis; ELISA = enzyme-linked immunosorbent assay; FVC = forced vital capacity; HLA = human leukocyte antigen; IB = immunoblotting; ID = immunodiffusion; IIF = indirect immunofluorescence; IP = immunoprecipitation; lcSSc = limited cutaneous systemic sclerosis; MCTD = mixed connective tissue disease; PFT = pulmonary function tests; PM = polymyositis; PM/SSc = myositis/scleroderma overlap; RLD = restrictive lung disease; RNP = ribonucleoprotein; SLE = systemic lupus erythematosus; snRNP = small nuclear RNP; SSc = systemic sclerosis. Arthritis Research & Therapy Vol 5 No 2 Ho and Reveille IntroductionSystemic sclerosis (scleroderma or SSc) is a heterogeneous disorder characterized by autoantibody subsets, which in turn have their own clinical associations. Much controversy resides in whether these autoantibodies contribute directly to the pathology seen in SSc or whether they are merely epiphenomena of the underlying disease process. Nevertheless, various autoantibodies found in patients with SSc carry significant value in diagnosis and in predicting clinical outcomes (Fig. 1). The autoantibodies classically associated with SSc include anti-centromere antibodies (ACA) and anti-Scl-70 (otherwise known as antitopoisomerase I or anti-topo I). In addition to these is the less commonly occurring anti-nucleolar antibody (ANoA) system, which comprises a mutually exclusive heterogeneous group of autoantibodies that produce nucleolar stain- AbstractScleroderma (systemic sclerosis) is associated with several autoantibodies, each of which is useful in the diagnosis of affected patients and in determining their prognosis. Anti-centromere antibodies (ACA) and anti-Scl-70 antibodies are very useful in distinguishing patients with systemic sclerosis (SSc) from healthy controls, from patients with other connective tissue disease, and from unaffected family members. Whereas ACA often predict a limited skin involvement and the absence of pulmonary involvement, the presence of anti-Scl-70 antibodies increases the risk for diffuse skin involvement and scleroderma lung disease. Anti-fibrillarin autoantibodies (which share significant serologic overlap with anti-U3-ribonucleoprotein antibodies) and anti-RNA-polymerase autoantibodies occur less frequently and are also predictive of diffuse skin involvement and systemic dise...

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Section: Other Autoantibodiesmentioning

confidence: 99%

Untitled

Reveille

2003

Arthritis Res Ther

183

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“…In some instances, these sera are still the exclusive tools for tracing cellular structures. This is the case for microtubule-organizing centers such as kinetochores (4)(5)(6) and centrosomes (7)(8)(9)(10). Among the anti-centrosome sera, some have immunoglobulins with a specificity toward antigenic determinants that are highly conserved from plants to mammals.…”

mentioning

confidence: 99%

“…In some instances, these sera are still the exclusive tools for tracing cellular structures. This is the case for microtubule-organizing centers such as kinetochores (4-6) and centrosomes (7)(8)(9)(10) Serum. In the course of a study on the inflammatory process, eight rabbits were injected with Streptococcus type 24 (17).…”

mentioning

confidence: 99%

Centrosomal proteins and lactate dehydrogenase possess a common epitope in human cell lines.

Gosti¹,

Marty²,

Courvalin³

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

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A spontaneously arising rabbit anti-centrosome serum with strong human specificity, used to identify specific antigens in isolated centrosomes, was shown to react with several noncentrosomal proteins including a 36-kDa protein that appeared to be the major cellular antigen. To explore the immunological relationship between noncentrosomal and centrosomal antigens, immunoglobblins were affimity purified using the individual noncentrosomal antigens (from lymphoblastoma KE37 cells) and were tested for their capacity to bind to human centrosomes in situ and to proteins from isolated centrosomes. In this way, the 36-kDa antigen, an abundant cytosolic protein, was shown to share at least one antigenic determinant with high molecular weight centrosomal proteins. This antigen was further identified by mild proteolysis as the glycolytic enzyme lactate dehydrogenase. In all the analyzed human cell lines, the centrosomal staining in situ was correlated with a strong labeling of purified lactate dehydrogenase in immunoblots. Conversely, the absence of centrosomal staining in rodent cells was always correlated with the absence of lactate dehydrogenase labeling. These data suggest an evolutionary relationship between centrosomal proteins and this "housekeeping" enzyme.Several cytoskeletal components have been studied at the cellular and molecular level (1-3), or even discovered (4), with nonimmune sera. In some instances, these sera are still the exclusive tools for tracing cellular structures. This is the case for microtubule-organizing centers such as kinetochores (4-6) and centrosomes (7)(8)(9)(10) Serum. In the course of a study on the inflammatory process, eight rabbits were injected with Streptococcus type 24 (17). When tested on cultured cells from various origins by the indirect immunoperoxidase technique, the preimmune serum of one rabbit (serum 0013) was shown to strongly label centrosomes and weakly label nucleoli in primate cells (12). The experimental immunization induced a strong and transient increase of this preimmune specificity. The fact that cellular labeling did not disappear after extensive preabsorption of the serum with Streptococcus type 24 showed that these specificities were antigenically unrelated to the Streptococcus (17). Moreover, these specificities were not detected in the sera of the seven rabbits immunized in the same way.Immunofluorescence Microscopy. Cells were fixed in PBS (150 mM NaCl/10 mM sodium phosphate, pH 7.4) containing 3% (vol/vol)

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“…Three of the 4 patients had SSc; the fourth had RP and telangiectasia. Moroi et al [16] reported anticentriole anti body in 2 of 100 (2%) patients with SSD, 1 patient with SSc and another who had RP and arthralgia. Three patients with anticentriole antibody have been reported in the litera ture, the first patient with SSc, the second with hyperthyroi dism and the third with RP alone [ 17.…”

Section: Discussionmentioning

confidence: 99%

“…At present, anticentromere antibody (ACA) is generally con sidered to be a serological marker of a mild form of SSc [8][9][10][11][12][13]. Antibody to centriole was first reported by Brenner et al [14], and, since then, only 9 patients with this anti body have been reported in the literature [15][16][17][18]. The clin ical distribution of anticentriole antibody has not yet been determined, although almost half of the reported patients had SSc.…”

Section: Introductionmentioning

confidence: 99%

Antibodies to Centromere and Centriole in Scleroderma Spectrum Disorders

et al. 1994

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The importance of early detection of scleroderma spectrum disorders (SSD) has been emphasized. We determined the clinical distribution of anticentromere antibody (ACA) and anticentriole antibody in the following four groups: (1) 264 patients with SSD, including 193 with systemic sclerosis, 29 with mixed connective tissue disease and 42 with suspected secondary Raynaud’s phenomenon (RP); (2) 26 patients with primary RP; (3) 248 patients with other connective tissue diseases, and (4) 139 patients with other skin diseases. The frequency of ACA was significantly higher in SSD (78/264, 30%) than in the other groups. In patients with SSD, the incidence of ACA in suspected secondary RP (28/42, 67%) was similar to that in type I systemic sclerosis (24/36, 67%). Anticentriole antibody was detected in only 1 patient with suspected secondary RP (0.4%) out of the 264 SSD patients. These data indicate that anticentriole antibody is very rare and that the antibodies against mitosis-related antigens such as centromere and centriole are associated with early SSD.

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Human anticentriole autoantibody in patients with scleroderma and Raynaud's phenomenon

Cited by 39 publications

References 12 publications

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Centrosomal proteins and lactate dehydrogenase possess a common epitope in human cell lines.

Antibodies to Centromere and Centriole in Scleroderma Spectrum Disorders

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