ArticleClinical and experimental immunology1991
Alveolar macrophages from patients with bronchogenic carcinoma and sarcoidosis similarly express monocyte antigens.
Article in Clinical and experimental immunology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 24 citations in OpenAlex.
- The respiratory DC/macrophage network at steady-state and upon influenza infection in the swine biomedical model.Mucosal immunology · 2016Article
- Resident alveolar macrophages are susceptible to and permissive of Coxiella burnetii infection.PloS one · 2012Article
- Role of soluble factors and three-dimensional culture in in vitro differentiation of intestinal macrophages.World journal of gastroenterology · 2007Article
- Isolation and phenotypic characterization of colonic macrophages.Clinical and experimental immunology · 1998Article
- Immunophenotyping of bronchoalveolar lavage lymphocytes.Clinical and diagnostic laboratory immunology · 1998Review
- Enrichment and characterization of dendritic cells from human bronchoalveolar lavages.Clinical and experimental immunology · 1994Article
- Adhesion molecules in lung diseases.Lung · 1994Review
- Increased CD11/CD18 expression on peripheral blood leucocytes of patients with sarcoidosis.Clinical and experimental immunology · 1992Article
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3 authors at 1 institution in 1 country.
Funding
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Abstract
It has been shown that bronchoalveolar lavages (BALs) from patients with sarcoidosis and other interstitial lung diseases contain abnormally increased numbers of alveolar macrophages (AM) expressing antigens found on monocytes. The aim of this study was to compare the phenotype of AM from patients with sarcoidosis with those from patients with non-interstitial lung disease, namely carcinoma. Using a panel of monoclonal antibodies against cells of the mononuclear phagocytic series and immunohistochemical staining, we have compared the expression of antigens on AM recovered at BAL and peripheral blood monocytes from patients with sarcoidosis, with similar cell preparations from bronchogenic carcinoma patients and normal volunteers. We have shown that CD14, CR1 (CD35) and CR3 (CD11b, CD18) are expressed on the majority of monocytes from all subjects, but on only a minority of normal AM. In both patients with sarcoidosis and patients with bronchogenic carcinoma increased proportions of AM expressed these monocyte-associated antigens. Since BALs from the carcinoma patients were derived from lung lobes which were radiologically free of tumour, the accumulation of AM expressing monocytic antigens is not a local response to the tumour. We conclude that infiltration of the lung with monocytes is a more general response to lung disease than has hitherto been reported.
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