[Changes in the systemic immunologic response in association with endometriosis using an animal model].
BACKGROUND
Endometriosis constitutes the growth of endometrial tissue in a place other than the uterine cavity. Its etiopathogenesis is unknown, although there is some evidence associating it with the decrease of cytotoxic activity in the immunological system.


OBJECTIVE
Evaluating the relationship between the development of ectopic endometrial tissue and the immunological status, and enumerating lymphocyte subpopulations and cytokine synthesis in T lymphocytes, using a murine endometriosis model.


METHODS
Spleen lymphocytes isolated from two study groups of 10 female mice of the Balb/c strain that had been submitted to the surgical implantation of autologous endometrial tissue in the peritoneal cavity, and sacrificed after 5 (group I) and 8 (group II) weeks, were incubated--or not--with PMA/lonomicine. Lymphocyte T numbers and their cytokine production were determined by flow cytometry.


RESULTS
A lower dispersion of the ectopic tissue growth value was observed in group II (24% vs. 42%). A smaller population of cytotoxic T lymphocytes and a greater IL-4 production in the stimulated cells of the study group (p < 0.05) were observed, as compared to the control group.


CONCLUSIONS
The presence of endometrial tissue in the uterine cavity decreases the amount of cytotoxic T lymphocytes and increases IL-4 production in total T lymphocytes, suggesting a modulation of the systemic immunological response to TH-2.
Hernández Guerrero
Cesar Angel
CA
Vadillo Ortega
Felipe
F
Tlapanco Barba
Rubén
R
Arriaga Pizano
Lourdes
L
Cérbulo Vázquez
Arturo
A
González Jiménez
Marco Antonio
MA
Beltrán Montoya
Jorge
J
D000818:Animals; D004715:Endometriosis / Q000276:immunology*; D005260:Female; D007111:Immunity, Cellular; D007371:Interferon-gamma / Q000378:metabolism*; D016753:Interleukin-10 / Q000378:metabolism; D007376:Interleukin-2 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D023421:Models, Animal; D016176:T-Lymphocyte Subsets; D013601:T-Lymphocytes / Q000276:immunology*
D007376:Interleukin-2; D007378:Interleukins; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma
Alteración de la respuesta inmunológica sistémica en asociación con endometriosis, empleando un modelo de estudio animal.