Suppression by progesterone of nonspecific in vitro lymphocyte stimulation in mice as a mechanism for the enhancement of herpes simplex virus type 2 vaginal infection.
The role of antibody, interferon, and cell-mediated immunity (CMI) were studied to determine the mechanisms for progesterone enhancement of vaginal herpes simplex virus type 2 (HSV 2) infection in mice. Three groups of mice were studied: nonpregnant control, pregnant, and nonpregnant progesterone-treated mice. Vaginal infection with HSV 2 did not elicit a neutralizing antibody or a systemic interferon response in any of the groups tested. Splenic lymphocytes from noninfected and infected mice were stimulated in vitro with a nonspecific T-cell mitogen concanavalin (Con A) to measure the proliferative phase of CMI in these groups of mice. No suppression of (3H) thymidine (3HTdR) uptake was found in the pregnant or nonpregnant, progesterone-treated animals as compared to nonpregnant control mice. When progesterone was added directly to the splenic lymphocytes and continuously present during Con A stimulation a statistically significant depression of 3HTdR incorporation was found. We concluded that progesterone depresses Con A stimulation of murine lymphocytes, but progesterone must be continuously present to do so.
D000818:Animals; D000914:Antibodies, Viral / Q000032:analysis; D003208:Concanavalin A / Q000037:antagonists & inhibitors; D004305:Dose-Response Relationship, Drug; D005260:Female; D006561:Herpes Simplex / Q000276:immunology*; D007111:Immunity, Cellular / Q000187:drug effects*; D007372:Interferons / Q000032:analysis; D008213:Lymphocyte Activation; D051379:Mice; D006559:Pemphigoid Gestationis / Q000276:immunology; D011247:Pregnancy; D011374:Progesterone / Q000494:pharmacology*; D018139:Simplexvirus / Q000276:immunology*; D014623:Vaginal Diseases / Q000276:immunology
D000914:Antibodies, Viral; D003208:Concanavalin A; D011374:Progesterone; D007372:Interferons