title: Dendritic cells attenuate the early establishment of endometriosis-like lesions in a murine model.
abstract: Complex interplay of innate and adaptive immune cells has been implicated in the establishment, maintenance, and progression of endometriosis. Defining the identity, activation state, and functional role of immune cells during lesion establishment will provide invaluable insight into the underlying mechanisms of disease. This study utilized a transgenic mouse model with conditional dendritic cell (DC) depletion (diphtheria toxin-treated B6.FVB-Itgax-hDTR-EGFP(tg)) and multiparametric flow cytometry to examine immune cell composition and activation state and to assess the functional role of DCs in endometriosis-like lesions. T cells and DCs were increased in lesions compared to native uteri and control splenocytes and demonstrated an activated phenotype (P < .05). Lesions in DC-depleted hosts demonstrated greater size (P < .001) and reduced expression of T-cell activation marker CD69 compared to controls (P < .05). Collectively, these results suggest that activated DCs within lesions activate T cells and result in the impairment of early lesion establishment.
authors.affiliation: Vincent Department of Obstetrics and Gynecology, Vincent Center for Reproductive Biology, Massachusetts General Hospital, Boston, MA, USA Department of Obstetrics, Gynecology, and Reproductive Biology, Harvard Medical School, Boston, MA, USA.
authors.forename: Aleksandar K
authors.initials: AK
authors.lastname: Stanic
authors.affiliation: Vincent Department of Obstetrics and Gynecology, Vincent Center for Reproductive Biology, Massachusetts General Hospital, Boston, MA, USA.
authors.forename: Minji
authors.initials: M
authors.lastname: Kim
authors.affiliation: Vincent Department of Obstetrics and Gynecology, Vincent Center for Reproductive Biology, Massachusetts General Hospital, Boston, MA, USA Department of Obstetrics, Gynecology, and Reproductive Biology, Harvard Medical School, Boston, MA, USA astyer@partners.org.
authors.forename: Aaron K
authors.initials: AK
authors.lastname: Styer
authors.affiliation: Vincent Department of Obstetrics and Gynecology, Vincent Center for Reproductive Biology, Massachusetts General Hospital, Boston, MA, USA Department of Obstetrics, Gynecology, and Reproductive Biology, Harvard Medical School, Boston, MA, USA brueda@partners.org.
authors.forename: Bo R
authors.initials: BR
authors.lastname: Rueda
mesh_terms: D000818:Animals; D002452:Cell Count / Q000379:methods; D003713:Dendritic Cells / Q000276:immunology* / Q000473:pathology*; D004195:Disease Models, Animal; D004715:Endometriosis / Q000276:immunology* / Q000473:pathology*; D005260:Female; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D013997:Time Factors
keywords: T cells; dendritic cells; endometriosis; immunocompetent syngeneic mouse model