Intraepithelial leukocytes in endometriosis and adenomyosis: comparison of eutopic and ectopic endometrium with normal endometrium.
Intraepithelial leukocytes (IEL) are recognized as an important component of most mucosal surfaces but have received scant attention in the human female reproductive tract. The aim of the present study was to characterize, quantify and compare IEL populations in normal endometrium (n = 30) and in eutopic and ectopic (endometriotic or adenomyotic lesions) endometrium from women with endometriosis (n = 30) or adenomyosis (n = 15) at different menstrual cycle phases in order to assess the role of IEL in these common but poorly understood disorders. IEL populations were examined in formalin-fixed, paraffin-embedded sections using a streptavidin-biotin-peroxidase complex technique and quantified in relation to epithelial cell numbers. IEL in control endometrium and eutopic endometrium in endometriosis and adenomyosis varied during the menstrual cycle, with CD45+, CD43+ and CD56+ cells increasing from the proliferative to the late secretory phase. IEL were elevated in surface compared with glandular epithelium in the proliferative and early secretory phases. Throughout the menstrual cycle there were no significant differences in IEL between eutopic and ectopic endometrium in adenomyosis. Endometriotic foci, however, contained elevated levels of CD45+, CD3+ and CD8+ cells and reduced numbers of CD56 + cells compared with the corresponding eutopic endometrium and these did not vary with menstrual cycle phase. In contrast, ectopic endometrium in adenomyosis showed some cyclical changes with CD56+ cells increasing significantly in the late secretory phase. It is possible these differences may play a role in the pathogenesis of endometriosis and the associated complications.
Bulmer
J N
JN
Department of Pathology, University of Newcastle, Newcastle upon Tyne, The Medical School, UK.
Jones
R K
RK
Searle
R F
RF
D000911:Antibodies, Monoclonal; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D017252:CD3 Complex / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D016022:Case-Control Studies; D004715:Endometriosis / Q000150:complications / Q000276:immunology / Q000473:pathology*; D004717:Endometrium / Q000276:immunology / Q000473:pathology*; D004848:Epithelium / Q000276:immunology / Q000473:pathology; D005260:Female; D006801:Humans; D007247:Infertility, Female / Q000209:etiology; D007694:Killer Cells, Natural / Q000276:immunology / Q000473:pathology; D017493:Leukocyte Common Antigens / Q000378:metabolism; D007958:Leukocyte Count; D007962:Leukocytes / Q000276:immunology / Q000473:pathology*; D051917:Leukosialin; D008597:Menstrual Cycle / Q000276:immunology; D012795:Sialoglycoproteins / Q000378:metabolism; D000097382:CD68 Molecule
D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017252:CD3 Complex; D017493:Leukocyte Common Antigens; D051917:Leukosialin; D012795:Sialoglycoproteins; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C465014:SPN protein, human