Objective To identify novel autoantibodies specific for dermatomyositis (DM), especially those specific for clinically amyopathic DM (C‐ADM). Methods Autoantibodies were analyzed by immunoprecipitation in 298 serum samples from patients with various connective tissue diseases (CTDs) or idiopathic pulmonary fibrosis (IPF). Antigen specificity of the sera was further examined by immunoblotting and indirect immunofluorescence (IF). The disease specificity and clinical features associated with the antibody of interest were determined. Results Eight sera recognized a polypeptide of ∼140 kd (CADM‐140 autoantigen) by immunoprecipitation and immunoblotting. Immunoreactivity was detected in the cytoplasm, and indirect IF revealed a granular or reticular pattern. Anti–CADM‐140 antibodies were detected in 8 of 42 patients with DM, but not in patients with other CTDs or IPF. Interestingly, all 8 patients with anti–CADM‐140 antibodies had C‐ADM. Among 42 patients with DM, those with anti–CADM‐140 autoantibodies had significantly more rapidly progressive interstitial lung disease (ILD) when compared with patients without anti–CADM‐140 autoantibodies (50% versus 6%; P = 0.008). Conclusion These results indicate that the presence of anti–CADM‐140 autoantibodies may be a novel marker for C‐ADM. Further attention should be directed to the detection of rapidly progressive ILD in those patients with anti–CADM‐140 autoantibodies.

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We have investigated the effect of plasma fibronectin (Fn) on binding and phagocytosis of sheep erythrocytes (E) by human peripheral blood monocytes. Unopsonized E were not phagocytosed in the absence or presence of Fn, but Fn enhanced the phagocytosis of E bearing IgG. Sheep erythrocytes sensitized with IgM and C3b were ingested only when monocytes were exposed to Fn. The Fn enhancement of phagocytosis occurred for both fluid-phase and glass-adherent monocytes. Experiments in which Fn was washed out before mixing monocytes with opsonized E demonstrated that the Fn effect occurred because of interaction with the monocytes and not the opsonized particles. Chromatography of the Fn on Biogel A 1.5m showed that the phagocytosis-enhancing activity exactly co-chromatographed with the Fn protein. Fn did not increase the number of monocyte membrane receptors for the Fc fragment of monomeric IgG. We conclude that Fn enhances monocyte phagocytosis, not by binding to particles as a conventional opsonin, but by stimulating monocytes to ingest already opsonized particles more avidly.

A Marker for a Subset of Polymyositis with Interstitial Pulmonary Fibrosis SHUNJI YOSHIDA, MASASHI AKIZUKI, TSUNEYO MIMORI, HAJIME YAMAGATA, SHINICHI INADA, and MITSUO HOMMAThe clinical significance of antibodies to the Jo-1 antigen in connective tissue diseases was studied. Clinical diagnoses of I1 patients who had anti-Jo-1 antibody were: polymyositis 8, dermatomyositis 1, and overlap syndrome 2 (polymyositis-systemic lupus erythematosus 1, polymyositis-scleroderma 1). All the patients who had anti-Jo-1 antibody showed interstitial pulmonary fibrosis, and in 2 patients antiJo-1 antibodies were detected before the appearance of lung disease.Identification of antinuclear antibodies with defined specificities has diagnostic and prognostic value in connective tissue diseases (1-3). Recent studies reveal the presence of several precipitating antibody systems in polymyositis-dermatomyositis (PM-DM) in which immunologic abnormalities were previously considered to be infrequent (4-8). However, the results from several laboratories indicate that these serologic reactions have considerable heterogeneity, and their mutual relationships and clinical significance remain to be clarified (8).We have reported two distinct precipitating

Objective To address whether the γ haplotype at exon 3 of the SAA1 gene is directly associated with type AA amyloidosis or is merely in linkage with an unknown polymorphism that is primarily associated with disease risk, we examined the SAA1 gene for new polymorphisms. Methods We analyzed DNA samples from 44 rheumatoid arthritis (RA) patients with AA amyloidosis (amyloid group), 55 RA patients without AA amyloidosis (RA group), and 58 non‐RA healthy subjects (non‐RA group). We also examined DNA samples from 50 Caucasians to compare linkage disequilibrium relationships involving SAA1 region polymorphisms between Japanese and Caucasoid populations. Results We observed 3 novel single‐nucleotide polymorphisms (SNPs) in the 5′‐flanking region of SAA1: −61C/G, −13T/C, and −2G/A. Comparison of allele frequencies and ratios of individuals with particular alleles between the study groups revealed statistically significant differences between the amyloid and RA groups and between the amyloid and non‐RA groups. Statistical analysis revealed that the −13T/C SNP was strongly associated with AA amyloidosis. In addition, we found tight linkage between the −13T allele and the α haplotype, rather than the β haplotype, at exon 3 in the Caucasoid population, while −13T was closely linked to the γ and β haplotypes, rather than the α haplotype, in the Japanese population. Since the linkage disequilibrium relationship was reversed between the Japanese and Caucasoid populations, different exon 3 haplotypes of SAA1 are found to be associated with the risk of AA amyloidosis in different ethnic groups. Conclusion Our data suggest that the SAA1 −13T allele, rather than SAA1 exon 3 haplotypes, is primarily associated with AA amyloidosis risk.