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• W2042704857 abstract "Introduction The mucosal immune system is present throughout the female reproductive tract1. Unlike other mucosal surfaces such as the intestine, the reproductive tract is unique in its exposure to antigens. For example, the upper female reproductive tract (uterus and fallopian tubes) is periodically exposed to allogeneic sperm or to a fetal–placental unit that is immunologically distinct. In contrast, the lower reproductive tract (cervix and vagina) has a bacterial ecosystem that contributes to reproductive health2. Moreover, the dynamic interactions between the lower and upper reproductive tract are unique in that vaginal contents (bacteria, sperm, dyes, etc.) enter the upper reproductive tract, irrespective of reproductive status, whereas secretions of the uterus, fallopian tubes and peritoneal cavity bathe the lower reproductive tract. To meet these diverse challenges, the mucosal immune system within the uterus, cervix and vagina is precisely controlled by the female sex hormones to optimize both maternal and fetal survival3. The overall objective of our studies is to define the role of sex hormones in regulating the mucosal immune system in the human female reproductive tract. By defining the mechanisms whereby sex hormones influence phenotype, immune function, and susceptibility to HIV infection, our intent is to contribute to a foundation of knowledge essential to prevent and control the spread of STI including HIV, the causative agent of AIDS4, which compromise women's reproductive health and survival. Antigen Presentation Mucosal surfaces of the body contain several types of antigen presenting cells that respond to potential pathogens5,6. For example, macrophages, B lymphocytes, dendritic cells, keratinocytes, Langerhans cells and epithelial cells have been shown to present antigen. Antigen presentation involves the internalization and processing of exogenous antigen to immunogenic fragments that are then presented in combination with either MHC class I or class II molecules to T lymphocytes. In previous studies7, we examined mixed cell suspensions from throughout the reproductive tract and found that they contained cells capable of presenting foreign antigen to autologous T cells. To characterize more fully the immune system in the human female reproductive tract, uterine epithelial and stromal cells from hysterectomy patients were purified to assess the capacity of these cells to present antigen. Irradiated epithelial cells co-cultured with T cells and tetanus toxoid induced syngeneic T-cell proliferation in comparison with cultures without tetanus toxoid8. Proliferation was significant, indicating that both purified epithelial cells and stromal cells were capable of antigen presentation to autologous T cells. Uterine Bactericidal Activity As the adaptive immune system at mucosal surfaces may take days to be activated and be effective against pathogens, initial innate protective mechanisms are available and are essential for health9. One such mechanism is the production of soluble factors by female reproductive tract epithelial cells that inhibit the growth of microorganisms. Among the epithelial cell secretions with known bactericidal effects are defensins, secretory leukocyte protease inhibitor (SLPI), the enzymes lysozyme and lactoferrin, tracheal antimicrobial peptide, and numerous other small peptides10. We have focused on innate immune protection by growing polarized uterine epithelial cells on cell inserts to examine whether these cells express soluble factors with antibacterial activity11. Apical rinses from polarized epithelial cells recovered from women at the proliferative and secretory stages of the menstrual cycle, but not from postmenopausal women, were equally effective in killing Staphylococcus aureus and Escherichia coli. As a part of these studies, we found that SLPI concentrations of apical washes from premenopausal women were significantly higher than those obtained from postmenopausal women. Furthermore, SLPI production correlated with bactericidal activity with respect to menstrual status and time in culture, and anti-SLPI antibody significantly decreased bactericidal activity from premenopausal epithelial cell rinses. These studies extend the findings of others, showing that the expression of SLPI varies in cervical mucus during the menstrual cycle, increases in amniotic fluid during gestation and labor12, and is released by cervical tissue in response to progesterone13. King et al.14 reported that the primary site of SLPI synthesis in the endometrium and decidua was the glandular epithelium, and tissues derived from women in the late secretory phase produced higher SLPI levels than tissues obtained from women in the proliferative phase. Taken together, these findings suggest that sex hormones play a regulatory role in innate immune protection. HIV Receptor Expression in the Uterus The recognition that heterosexual transmission of HIV-1 accounts for 70–80% of new infections worldwide, with 80% occurring from men to women15, prompted us to examine the possibility that the upper female reproductive tract might be a potential site of HIV infection. Chemokine receptors are recognized as essential co-receptors for HIV infection and are expressed on several types of hematopoietic and non-hematopoietic cells, including epithelial cells16,17. CCR5 was identified as a major co-receptor for macrophage-tropic (M-tropic) non-syncytium-inducing strains of HIV-1 because infection is blocked by the presence of the CCR5 ligands MIP-1α, MIP-1β and RANTES18. Similarly, CXCR4 was identified as the major co-receptor for infection by T-tropic, syncytium-inducing strains of HIV-1, as infection by these strains of HIV-1 is blocked by the CXCR4 ligand stromal-derived factor type 118. In previous studies, we found that primary epithelial cells from the uteri of women undergoing hysterectomies were readily infected by HIV-119. These findings prompted us to use confocal laser microscopy to evaluate the expression of HIV receptors and co-receptors on uterine epithelia at different stages of the menstrual cycle20. CD4, CCR5, and CXCR4 were found on glandular and luminal epithelial cells. Both CCR5 and CXCR4 expression increased during the proliferative phase of the menstrual cycle, CCR5 expression was reduced during the secretory phase, whereas CXCR4 expression was not reduced. The variation in expression of these receptors during the menstrual cycle suggests that receptors are regulated by the sex hormones estradiol and progesterone during the menstrual cycle20. These results provide evidence that the uterus, and potentially the entire upper reproductive tract, may be an important site for the initial events involved in HIV infection. Furthermore, these findings suggest that endocrine changes during the menstrual cycle play a crucial role in influencing the susceptibility of cells within the female reproductive tract to HIV infection. Conclusion The results presented demonstrate the complexities of the innate and adaptive immune systems in the reproductive tract, and indicate that the mucosal immune system is under hormonal control. These studies should increase our presently limited understanding of the mucosal immune system in the reproductive tract, and contribute to the basis of knowledge essential for the prevention of local infection in the genital mucosa, the management of STI and insight into the heterosexual transmission of HIV-1. Support This study was supported by NIH grants AI 51877 and AI 13541." @default.
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• W2042704857 title "Effect of the Menstrual Cycle on Immunological Parameters in the Human Female Reproductive Tract" @default.
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• W2042704857 doi "https://doi.org/10.1097/01.qai.0000167040.58181.d5" @default.
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