Hi Everyone,
Recently we tried to evaluate the frequency of CD20+ B-cells in human lungs. We collected around 30mg of human lung tissue, digested the cells and then measured B-cells by flow cytometry. We found around 0.5% of viable CD45+ cells stained positively for CD20. Does anyone have any data that supports or refutes these frequencies?
Thanks,
Victor
Dear Mr. Ferreira,
in human lungs B cells are mainly located within bronchus associated lymphoid tissue (BALT) that is not found in healthy human lungs. Nevertheless induced BALT (iBALT) is commonly found in various diseases. I would say that it would be important to know exact location of the sample and patients' history, perhaps perform control histology, in order to be aware of lung-sample status.
Plasmacells are CD20 (MS4A1) negative.
Alveolar macrophages (CD45+) can be rather abundant in pulmonary tissue, specially in some conditions (smoking).
Kind regards
Snježana Čužić
https://www.ncbi.nlm.nih.gov/pubmed/21034975
https://openi.nlm.nih.gov/detailedresult.php?img=PMC3767487_cmar-5-225Fig1&req=4
http://www.proteinatlas.org/ENSG00000156738-MS4A1/tissue/lung
https://atlasantibodies.com/#!/products/MS4A1-antibody-HPA014341
Using a murine model, we demonstrated that endobronchial administration of antibodies (Abs) to MHC class I results in cellular infiltration, epithelial metaplasia, fibrosis and obstruction of the small airways (Obliterative Airway Disease (OAD)) mediated predominantly by Th17 responses to self-antigens. This resembles bronchiolitis obliterans syndrome developed following human lung transplantation. Since B cells play a crucial role in induction of autoimmune responses, we defined the role of B cells and its antigen presenting properties in induction of OAD in this study. Anti-MHC class I was administered endobronchially in B−/− and wild type mice. In contrast to wild type, B−/− animals did not demonstrate cellular infiltration, epithelial metaplasia and obstruction of airways following anti-MHC. Frequency of Kα1-tubulin and CollagenV specific IL-17 cells was significantly decreased in B−/− mice. As expected, Abs against self-antigens and germinal center formation were not developed in B−/− mice. Thus we conclude that B cells and its antigen presenting capacity play an important role in induction of immune responses to self-antigens and immunopathogenesis of OAD following administration of anti-MHC. Therefore, strategies to block B cell and its antigen presenting functions should be considered for preventing the development of chronic rejection.
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