[The pathogenic role of ACPA in rheumatoid arthritis].

Abstract

  In rheumatoid arthritis (RA), ACPA (anti-citrullinated protein/peptide antibody) is elevated with high specificity, and clinically, anti-CCP (cyclic citrullinated peptide) antibody is widely used for diagnosis of RA. It is thought ACPAs are produced with genetic background such as HLA-DR, environmental factors such as periodontal disease and smoking, however, the pathogenic role of ACPA in RA has not been elucidated. These were showed immune complexes including ACPA or ACPA itself promoted inflammatory cytokine production such as TNF. PADs (peptidylarginine deiminases) were expressed and citrullinated proteins existed in RA synovium. ACPAs were deposited on the site of citrulline in CD68 positive cells of RA synovium. The damage of bone and cartilage is observed in RA. It was also suggested that deposition of ACPAs caused osteoclastogenesis and bone loss. We introduce several findings about the pathogenic role of ACPA in RA.

• Authors: Naoto Umeda, Isao Matsumoto, Takayuki Sumida
• Journal: Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology (Nihon Rinsho Meneki Gakkai Kaishi) Vol. 40 Issue 6 Pg. 391-395 ( 2017) ISSN: 1349-7413 [Electronic] Japan
• PMID: 29367523 (Publication Type: Journal Article, Review)

Chemical References

• Anti-Citrullinated Protein Antibodies
• Antigens, CD
• Antigens, Differentiation, Myelomonocytic
• CD68 antigen, human
• HLA-DR Antigens
• Inflammation Mediators
• Tumor Necrosis Factor-alpha
• Citrulline
• Protein-Arginine Deiminases

Topics

• Anti-Citrullinated Protein Antibodies (adverse effects, immunology)
• Antigens, CD
• Antigens, Differentiation, Myelomonocytic
• Arthritis, Rheumatoid (diagnosis, immunology, metabolism, pathology)
• Bone Resorption (immunology)
• Bone and Bones (pathology)
• Cartilage (pathology)
• Citrulline (immunology, metabolism)
• HLA-DR Antigens
• Humans
• Inflammation Mediators (metabolism)
• Osteogenesis (immunology)
• Periodontal Diseases
• Protein-Arginine Deiminases (metabolism)
• Smoking
• Synovial Membrane (cytology, metabolism)
• Tumor Necrosis Factor-alpha (metabolism)