Extensive surface phenotyping of alveolar macrophages in interstitial lung disease

Marcia L. Taylor*, Paul W. Noble, Barbara White, Robert Wise, Mark C. Liu, Bruce S. Bochner

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


There is increasing evidence implicating activated macrophages in the pathogenesis of interstitial and other lung diseases. We investigated whether there was a unique pattern of cell surface expression that constituted a disease-specific phenotype on alveolar macrophages from patients with interstitial lung disease (ILD). Macrophage cell surface receptor expression of 19 selected markers was assessed by indirect immunofluorescence and flow cytometry in bronchoalveolar lavage (BAL) fluids from patients with idiopathic pulmonary fibrosis (IPF, n = 4), scleroderma (SCL-ILD, n = 14), mild asthma (n = 7), allergy without asthma (n = 2), and normal subjects (n = 9). There was increased expression of adhesion receptors (CD11c, CD29, CD36, CD44, CD49e, CD54), receptors involved in signal transduction and/or inflammation (CD13, CD45, CD53), and other markers (CD9, CD52, CD71, CD98, HLA Class I) on macrophages from ILD patients compared to the non-ILD group. Most markers upregulated on macrophages in ILD were significantly inversely correlated with clinical parameters of disease activity such as FEV1, FVC, and DL(CO) and positively correlated with numbers of BAL neutrophils and eosinophils. Increased expression of several cell surface markers suggests that activated alveolar macrophages may contribute to the pathophysiology of IPF and SCL-ILD.

Original languageEnglish (US)
Pages (from-to)33-41
Number of pages9
JournalClinical Immunology
Issue number1
StatePublished - Jan 2000


  • Alveolar macrophages
  • CD markers
  • Idiopathic pulmonary fibrosis
  • Interstitial lung disease
  • Phenotyping
  • Scleroderma

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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