title: Morphologic and quantitative assessment of CD20+ B cell infiltrates in rheumatoid arthritis-associated nonspecific interstitial pneumonia and usual interstitial pneumonia.
abstract: OBJECTIVE
  B lymphocytes are emerging as important elements in the events leading to joint destruction in rheumatoid arthritis (RA). However, B lymphocytes have not been studied in rheumatoid arthritis (RA)-associated lung disease. We performed a morphologic and quantitative analysis of B lymphocytes and plasma cells in RA-associated interstitial pneumonia (IP) in comparison with idiopathic IP and normal lungs.
  
  
  METHODS
  Open-lung biopsy specimens from patients with RA-associated IP (n = 18), patients with idiopathic IP (n = 21), and control subjects (n = 11) were stained with antibodies to CD20 and CD138. Morphologic patterns of stained specimens were characterized and staining was quantified using computer-assisted image analysis.
  
  
  RESULTS
  In RA-associated IP, marked follicular B cell hyperplasia was detected, which was limited almost entirely to peribronchiolar lymphoid aggregates. Plasma cells were also present in large numbers, but showed a more diffuse tissue infiltration. Quantification of B cells demonstrated higher cellularity in RA-associated IP (median 2.0%, interquartile range [IQR] 1.0-5.7) as compared with idiopathic IP (0.9%, IQR 0.5-2.1). Control specimens showed a significantly smaller number of B cells compared with both diseases (0.4%, IQR 0.1-1.3). In RA patients who were smokers and in those who were male, the proportion of CD20+ tissue areas further increased to 4.3% (IQR 1.0-5.8) and 3.9% (IQR 0.7-6.9), respectively.
  
  
  CONCLUSIONS
  We demonstrated a significant follicular B cell hyperplasia in RA-associated IP. The differences between RA-associated IP and idiopathic IP imply a differential emphasis of B cell-mediated mechanisms in the 2 diseases despite radiologic and histologic similarities and provide a rationale for studying functional aspects of B cell involvement in the pathogenesis of RA-associated IP.
authors.affiliation: Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.
authors.forename: Sarah R
authors.initials: SR
authors.lastname: Atkins
authors.forename: Carl
authors.initials: C
authors.lastname: Turesson
authors.forename: Jeffery L
authors.initials: JL
authors.lastname: Myers
authors.forename: Henry D
authors.initials: HD
authors.lastname: Tazelaar
authors.forename: Jay H
authors.initials: JH
authors.lastname: Ryu
authors.forename: Eric L
authors.initials: EL
authors.lastname: Matteson
authors.forename: Tim
authors.initials: T
authors.lastname: Bongartz
mesh_terms: D000328:Adult; D000368:Aged; D018951:Antigens, CD20 / Q000378:metabolism*; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000276:immunology / Q000473:pathology*; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D015415:Biomarkers / Q000378:metabolism; D001706:Biopsy; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008168:Lung / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D017563:Lung Diseases, Interstitial / Q000209:etiology / Q000276:immunology / Q000473:pathology*; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism; D008875:Middle Aged; D010950:Plasma Cells / Q000378:metabolism / Q000473:pathology; D011509:Proteoglycans / Q000378:metabolism; D012129:Respiratory Function Tests; D053668:Syndecan-1; D053667:Syndecans
chemical_list: D018951:Antigens, CD20; D015415:Biomarkers; D008562:Membrane Glycoproteins; D011509:Proteoglycans; C508241:SDC1 protein, human; D053668:Syndecan-1; D053667:Syndecans