title: Effect of menstrual cycle variation in female sex hormones on cellular immunity and regulation.
abstract: Ovarian steroid hormones reduce cell-mediated immunity (CMI), perhaps by increasing regulatory T cells. We examined the relationship of estrogen and progesterone plasma concentrations during the menstrual cycle with circulating regulatory T cells (Treg cells) and with varicella-zoster virus (VZV)-specific lymphocyte proliferation (VZV-LPA). Twenty healthy and 20 HIV-infected women were tested at 1-4, 10-14, and 20-24days of the menstrual cycle. HIV-infected women experienced significant increases in the frequency of peripheral blood CD4+IL10+ and CD8+FoxP3+ Treg cells from the early and late follicular phases to the luteal phase of their cycles. Healthy women experienced significant increases only in CD4+IL10+ Treg cells. The increase in CD4+IL10+ Treg cells between the late follicular and the luteal phases of HIV-infected and uninfected women significantly correlated with the corresponding increases in progesterone plasma concentrations. VZV-LPA results decreased from the early and late follicular phases to the luteal phase in both groups. The decrease in VZV-LPA results significantly correlated with the increase in CD4+IL10+ Treg cells underscoring the potential immunosuppressive effect of the progesterone-stimulated Treg cells. In conclusion, the increase in progesterone levels during the menstrual cycle was associated with higher Treg frequencies and lower CMI.
authors.affiliation: Department of Pediatrics, The University of Colorado Denver, School of Medicine, Aurora, CO 80045, USA. Adriana.Weinberg@ucdenver.edu
authors.forename: Adriana
authors.initials: A
authors.lastname: Weinberg
authors.forename: Laura
authors.initials: L
authors.lastname: Enomoto
authors.forename: Roland
authors.initials: R
authors.lastname: Marcus
authors.forename: Jennifer
authors.initials: J
authors.lastname: Canniff
mesh_terms: D000293:Adolescent; D000328:Adult; D000956:Antigens, Viral / Q000276:immunology; D015704:CD4 Antigens / Q000096:biosynthesis; D016827:CD8 Antigens / Q000096:biosynthesis; D005260:Female; D051858:Forkhead Transcription Factors / Q000096:biosynthesis; D006678:HIV / Q000276:immunology* / Q000472:pathogenicity; D015658:HIV Infections / Q000276:immunology* / Q000503:physiopathology; D014645:Herpesvirus 3, Human / Q000276:immunology*; D006801:Humans; D007111:Immunity, Cellular; D016753:Interleukin-10 / Q000378:metabolism; D008597:Menstrual Cycle / Q000097:blood / Q000276:immunology; D008875:Middle Aged; D011374:Progesterone / Q000097:blood; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism* / Q000473:pathology / Q000821:virology
chemical_list: D000956:Antigens, Viral; D015704:CD4 Antigens; D016827:CD8 Antigens; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D016753:Interleukin-10; D011374:Progesterone