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Relationship between Jo-1 B Cell Epitope Profile and Clinical Features of Anti-Synthetase Syndrome.
Yamaguchi, Koichi; Tang, Qi; LaConti, Joseph J; Kippelen, Fanny; Zhu, Lei; Poland, Paul; Hartoyo, Mara; Aggarwal, Rohit; Oddis, Chester V; Ascherman, Dana P.
Afiliación
  • Yamaguchi K; Gunma University Graduate School of Medicine, Gunma, Japan and University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.
  • Tang Q; Second Xiangya Hospital of Central South University, Changsha, China.
  • LaConti JJ; University of Miami School of Medicine, Miami, Florida.
  • Kippelen F; University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
  • Zhu L; University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
  • Poland P; University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
  • Hartoyo M; University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
  • Aggarwal R; University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
  • Oddis CV; University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
  • Ascherman DP; University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
ACR Open Rheumatol ; 6(10): 615-624, 2024 Oct.
Article en En | MEDLINE | ID: mdl-38973625
ABSTRACT

OBJECTIVE:

Anti-histidyl-transfer RNA synthetase (Jo-1) antibodies are associated with myositis as well as different extramuscular organ complications comprising the anti-synthetase syndrome. This study aimed to clarify the relationship between anti-Jo-1 epitope recognition patterns and specific clinical features of this syndrome.

METHODS:

B cell epitope mapping was performed via enzyme-linked immunosorbent assay in 180 patients who were anti-Jo-1 antibody-positive using overlapping peptides/protein fragments spanning the amino-terminal 151 amino acids of Jo-1 as substrate antigens. Statistical associations with clinical features were assessed through rank-sum, correlation, and cluster analyses.

RESULTS:

The level of reactivity against subfragments spanning amino acids 1-151 of Jo-1 paralleled that of full-length Jo-1, confirming the immunodominance of this amino-terminal region. The corresponding frequencies of reactivity to peptides 1 (amino acids [aa] 1-21), 3 (aa 27-47), 4 (aa 40-60), 10 (aa 118-138), and 11 (aa 131-151) were 6.1%, 42.5%, 6.8%, 6.7%, and 20.3%. While anti-full-length Jo-1 antibodies were significantly associated with Raynaud phenomenon, anti-fragment A2 (aa 1-60) and A3 (aa 1-90) antibodies were associated with proximal muscle weakness, Raynaud phenomenon, arthritis, and sicca syndrome. Anti-fragment A4 (aa 1-120) and A5 (aa 1-151) antibodies were also associated with sicca syndrome. Peptide 1 (aa 1-21) antibodies were associated with Raynaud phenomenon and dysphagia. Whereas anti-peptide 3 (aa 27-47) antibodies were also linked to Raynaud phenomenon, anti-peptide 9 (aa 105-125) antibodies were associated with mechanic's hands.

CONCLUSION:

Autoantibodies targeting different amino-terminal subfragments and/or peptides of Jo-1 were associated with specific clinical features of the anti-synthetase syndrome, demonstrating the biomarker potential of B cell epitope profiling in this disorder.

Texto completo: 1 Base de datos: MEDLINE Idioma: En Revista: ACR Open Rheumatol Año: 2024 Tipo del documento: Article

Texto completo: 1 Base de datos: MEDLINE Idioma: En Revista: ACR Open Rheumatol Año: 2024 Tipo del documento: Article