DEFICIENT CELLULAR-IMMUNITY IN ENDOMETRIOSIS
DEFICIENT CELLULAR-IMMUNITY IN ENDOMETRIOSIS
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DOI:
10.1016/0002-9378(81)90598-6
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发表时间:
1981-01-01
影响因子:
9.8
通讯作者:
BAKER, GF
中科院分区:
文献类型:
--
作者:
DMOWSKI, WP;STEELE, RW;BAKER, GF
Cell-mediated autoimmune responses were studied by in vivo and in vitro techniques in 5 rhesus monkeys with spontaneous endometriosis. The results were compared with similar data obtained from 5 normal rhesus monkeys without endometriosis. The in vivo studies included intradermal injection of autologous antigens prepared from uterine endometrium, ectopic endometrium or peritoneum, or injection of the mitogen, phytohemagglutinin (PHA). Skin biopsies were obtained at 48 h and evaluated under the light microscope for perivascular lymphocytic infiltration. The mean number of lymphocytes per high-power field after injection of the autologous endometrial antigen was significantly smaller in animals affected by endometriosis than in the control group. There was no significant difference in lymphocytic response to autologous peritoneal antigens between the groups. Animals of both groups responded readily to PHA with marked perivascular lymphocytic infiltration. Lymphocyte stimulation responses to the same autologous antigens or to PHA were evaluated by means of in vitro assays and micro-methods. Lymphocyte stimulation response to autologous endometrial antigens in the group with endometriosis was significantly less than in the control group. There was no significant difference in response to the peritoneal antigens between the groups; the response to PHA was marked in all animals of both groups. Rhesus monkeys with spontaneous endometriosis apparently have an altered cellular immune response to autologous antigens. Although the animals were immunologically competent, as judged by responses to PHA, in vivo and in vitro studies indicated a decrease in the cell-mediated immune response to autologous endometrial antigens. Endometrial cells translocated from their normal location may implant only in women with specific alteration in cell-mediated immunity. New light is thus shed on the cause of endometriosis.