Phenotypic characterization of infiltrating leukocytes in benign prostatic hyperplasia.
This study for the first time elaborates on cells of the immune system present in benign prostatic hyperplasia (BPH). Compared with normal prostate, all BPH-derived specimens revealed a marked increase of CD45+ leukocytes, characterization of which demonstrated three major cell types, i.e., CD3+ T lymphocytes, CD11c+ macrophages and CD20+ B lymphocytes. Frequencies of CD3+ cells/mm2 of cryocut sections were increased at least 10 times in BPH specimens, and the CD8+:CD4+ T suppressor/cytotoxic:T helper cell ratio was reversed. The infiltrating leukocytes predominantly populate the interstitium and accumulate around epithelial ducts which, however, were found to be invaded and/or destroyed only in a number of cases. Phenotypic alterations of surface antigen expression on prostate epithelial cells in BPH that might be due to the presence of lymphocytes were examined by using monoclonal antibodies (mAb) directed against human leukocyte antigens (HLA). Whereas anti-HLA-DR reactivity in normal prostate is restricted to small numbers of macrophages and includes neither prostate epithelial cells nor prostate T cells, it was found to be dramatically increased in BPH, comprising CD45+ cells and prostate epithelial cells as demonstrated by double-staining with anti-cytokeratin or anti-prostate-specific antigen. A mean of 40% of analyzed epithelial glands in BPH reacted with anti-HLA-DR, but not with anti-DQ or -DP monoclonal antibodies. A new method for the enrichment of prostate-derived lymphocytes was established to facilitate phenotypic analysis by flow cytometry, demonstrating 70 to 80% of enriched CD45+ cells to stain for CD3, approximately 60% thereof for CD4, 30% for CD8, and the remaining 10% with anti-CD20, a pan-B-cell marker. Flow cytometry showed that, in contrast to peripheral T cells, both CD4+ and CD8+ prostatic T cells were positive for the T cell activation markers HLA-DR and interleukin-2-receptor.
Department of Urology, University of Vienna Medical School, Austria.
G
G
Theyer
G
G
Kramer
I
I
Assmann
E
E
Sherwood
W
W
Preinfalk
M
M
Marberger
O
O
Zechner
G E
GE
Steiner
D000911:Antibodies, Monoclonal; D015703:Antigens, CD / Q000032:analysis; D018951:Antigens, CD20; D000944:Antigens, Differentiation, B-Lymphocyte / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D000951:Antigens, Neoplasm / Q000032:analysis; D000954:Antigens, Surface / Q000032:analysis; D001402:B-Lymphocytes / Q000737:chemistry / Q000276:immunology / Q000473:pathology; D018845:CD11 Antigens; D017252:CD3 Complex; D015815:Cell Adhesion Molecules / Q000032:analysis; D002465:Cell Movement; D004848:Epithelium / Q000737:chemistry / Q000276:immunology / Q000473:pathology; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D018799:Intercellular Adhesion Molecule-1; D007633:Keratins / Q000032:analysis; D007962:Leukocytes / Q000276:immunology* / Q000473:pathology*; D016246:Lymphocytes, Tumor-Infiltrating / Q000502:physiology*; D008264:Macrophages / Q000737:chemistry / Q000276:immunology / Q000473:pathology; D008297:Male; D010641:Phenotype; D011467:Prostate / Q000737:chemistry / Q000276:immunology / Q000473:pathology; D017430:Prostate-Specific Antigen; D011470:Prostatic Hyperplasia / Q000097:blood* / Q000473:pathology*; D011948:Receptors, Antigen, T-Cell / Q000032:analysis; D013601:T-Lymphocytes / Q000737:chemistry / Q000276:immunology / Q000473:pathology
D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D018951:Antigens, CD20; D000944:Antigens, Differentiation, B-Lymphocyte; D000945:Antigens, Differentiation, T-Lymphocyte; D000951:Antigens, Neoplasm; D000954:Antigens, Surface; D018845:CD11 Antigens; D017252:CD3 Complex; D015815:Cell Adhesion Molecules; D006684:HLA-DR Antigens; D011948:Receptors, Antigen, T-Cell; D018799:Intercellular Adhesion Molecule-1; D007633:Keratins; D017430:Prostate-Specific Antigen