Normal human peritoneal macrophages are unable to cap and internalize class II antigens

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AI-generated summary by claude@2026-08, 2026-08-02

Normal human peritoneal macrophages fail to cap and internalize HLA-DR, unlike endometriosis and other macrophages, possibly for scavenging functions without inflammation.

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Abstract

Normal human peritoneal macrophages show a restricted capacity to differentiate into inflammatory macrophages in vivo. We now report that these cells are unable to cap and internalize HLA-DR, as compared to endometriosis, and other macrophages. Immunoelectron microscopy indicated that lack of modulation was not due to the presence of preclustered antigenic sites. Northern blot analysis demonstrated transcripts for HLA.DR, c-fms, and c-fos, indicating that the surface defects were not likely to be associated with a general depression of transcriptional activity. There was no correlation between the mobility of class II molecules and the ability to present antigen as determined by autologous lymphocyte responses to tetanus toxoid. The inability of normal peritoneal macrophages to modulate class II antigens may represent a normal and more general environmental alteration required to permit peritoneal cells a scavenging function without developing the deleterious effects leading to a peritoneal inflammatory response.

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Condition tags

endometriosis

MeSH descriptors

Antigens, Surface HLA-D Antigens HLA-DR Antigens Immunologic Capping Macrophages Antibodies, Monoclonal Antigen-Presenting Cells Antigen-Presenting Cells Antigens, Surface Cross-Linking Reagents Endometriosis Endometriosis Endometriosis Endometriosis Female Flow Cytometry HLA-D Antigens HLA-DR Antigens Humans Macrophages

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