TY - JOUR
T1 - Enhanced Expression of Resident Leukocyte Interferon γ mRNA in Endometriosis
AU - KLEIN, NANCY A.
AU - PÉRGOLA, GABRIELA M.
AU - RAO‐TEKMAL, RAJESHWAR
AU - DEY, TAMMY D.
AU - SCHENKEN, ROBERT S.
N1 - Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 1993
Y1 - 1993
N2 - PROBLEM: Previous studies have shown that the endometrial epithelial/stromal cell proliferative activity of endometriosis is significantly less than that of normal endometrium and that the concentration of resident stromal leukocytes is significantly greater in ectopic than in eutopic endometrium. Other work has shown that interferon γ (IFNγ), secreted by resident leukocytes, inhibits endometrial cell proliferation in vitro. Accordingly, we hypothesized that the lower proliferative activity of endometriosis may be related to enhanced resident leukocyte IFN‐y production. This study was designed to assess whether resident leukocytes in endometriosis express IFNγ mRNA and to compare this expression to that of normal endometrium. METHODS: Biopsies of ectopic endometrium (N = 16) from women in the follicular phase and normal proliferative (N = 9) and secretory (N = 8) endometria were examined for IFNγ expression. Using monoclonal antibodies specific for CD45 (leukocyte common antigen), CD3 (a T‐cell marker) and CDI lc (a macrophage marker), leukocyte types were identified immunocytochemically, followed by in situ hybridization to examine expression of IFNγ mRNA. RESULTS: Results demonstrated that (1) the overall concentration of T cells and macrophages expressing IFN‐γ mRNA is significantly greater in endometriosis as compared to eutopic endometrium, and (2) the percent of each leukocyte type expressing IFNγ mRNA is greater in endometriosis than in normal endometrium. CONCLUSIONS: These findings support a possible paracrine role for resident leukocytes in regulating cell proliferation in endometriosis. 1993 Munksgaard
AB - PROBLEM: Previous studies have shown that the endometrial epithelial/stromal cell proliferative activity of endometriosis is significantly less than that of normal endometrium and that the concentration of resident stromal leukocytes is significantly greater in ectopic than in eutopic endometrium. Other work has shown that interferon γ (IFNγ), secreted by resident leukocytes, inhibits endometrial cell proliferation in vitro. Accordingly, we hypothesized that the lower proliferative activity of endometriosis may be related to enhanced resident leukocyte IFN‐y production. This study was designed to assess whether resident leukocytes in endometriosis express IFNγ mRNA and to compare this expression to that of normal endometrium. METHODS: Biopsies of ectopic endometrium (N = 16) from women in the follicular phase and normal proliferative (N = 9) and secretory (N = 8) endometria were examined for IFNγ expression. Using monoclonal antibodies specific for CD45 (leukocyte common antigen), CD3 (a T‐cell marker) and CDI lc (a macrophage marker), leukocyte types were identified immunocytochemically, followed by in situ hybridization to examine expression of IFNγ mRNA. RESULTS: Results demonstrated that (1) the overall concentration of T cells and macrophages expressing IFN‐γ mRNA is significantly greater in endometriosis as compared to eutopic endometrium, and (2) the percent of each leukocyte type expressing IFNγ mRNA is greater in endometriosis than in normal endometrium. CONCLUSIONS: These findings support a possible paracrine role for resident leukocytes in regulating cell proliferation in endometriosis. 1993 Munksgaard
KW - Cytokines
KW - in situ hybridization
KW - lymphoid cells
KW - proliferation
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U2 - 10.1111/j.1600-0897.1993.tb00605.x
DO - 10.1111/j.1600-0897.1993.tb00605.x
M3 - Article
C2 - 7906125
AN - SCOPUS:0027771871
SN - 1046-7408
VL - 30
SP - 74
EP - 81
JO - American Journal of Reproductive Immunology
JF - American Journal of Reproductive Immunology
IS - 2-3
ER -