Dendritic Cells Attenuate the Early Establishment of Endometriosis-Like Lesions in a Murine Model

article OA: closed CC0 ⤵ 38 in-corpus citations
AI-generated summary by claude@2026-06+body, 2026-06-07

Activated dendritic cells in endometriosis-like lesions impair early lesion establishment by activating T cells, as demonstrated by larger lesions in DC-depleted mice.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text

This study examined the role of dendritic cells (DCs) during early endometriosis-like lesion establishment using a conditional DC-depletion transgenic mouse model (diphtheria toxin-treated Itgax-hDTR mice) and multiparametric flow cytometry to assess immune cell composition and activation. Compared with native uteri and control splenocytes, endometriosis-like lesions showed increased T cells and DCs with an activated phenotype, and DC depletion resulted in larger lesions along with reduced expression of the T-cell activation marker CD69. The authors explicitly interpret these findings as activated DCs promoting T-cell activation and impairing early lesion establishment, while noting the functional readout is limited to early-stage lesion development and specific activation markers. This paper is centrally about endometriosis — it uses DC depletion to demonstrate how activated dendritic cells modulate early lesion establishment in a murine endometriosis-like model.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Full text 6,213 characters · extracted from oa-doi-fallback · 2 sections · click to expand

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-EGFPtg) 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. Similar content being viewed by others

References

Giudice LC, Kao LC. Endometriosis. Lancet. 2004;364(9447):1789–1799. Houston DE. Evidence for the risk of pelvic endometriosis by age, race and socioeconomic status. Epidemiol Rev. 1984;6:167–191. Simoens S, Hummelshoj L, D’Hooghe T. Endometriosis: cost estimates and methodological perspective. Hum Reprod Update. 2007;13(4):395–404. Olive DL, Pritts EA. Treatment of endometriosis. N Engl J Med. 2001;345(4):266–275. Sampson J. Peritoneal endometriosis due to menstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol. 1927;14:442–469. Burney RO, Giudice LC. Pathogenesis and pathophysiology of endometriosis. Fertil Steril. 2012;98(3):511–519. Barrier BF. Immunology of endometriosis. Clin Obstet Gynecol. 2010;53(2):397–402. Lebovic DI, Mueller MD, Taylor RN. Immunobiology of endometriosis. Fertil Steril. 2001;75(1):1–10. Garai J, Molnar V, Varga T, Koppan M, Torok A, Bodis J. Endometriosis: harmful survival of an ectopic tissue. Front Biosci. 2006;11(1):595–619. Eisermann J, Gast MJ, Pineda J, Odem RR, Collins JL. Tumor necrosis factor in peritoneal fluid of women undergoing laparoscopic surgery. Fertil Steril. 1988;50(4):573–579. Pizzo A, Salmeri FM, Ardita FV, Sofo V, Tripepi M, Marsico S. Behaviour of cytokine levels in serum and peritoneal fluid of women with endometriosis. Gynecol Obstet Invest. 2002;54(2):82–87. Hornung D, Bentzien F, Wallwiener D, Kiesel L, Taylor RN. Chemokine bioactivity of RANTES in endometriotic and normal endometrial stromal cells and peritoneal fluid. Mol Hum Reprod. 2001;7(2):163–168. Kalu E, Sumar N, Giannopoulos T, et al. Cytokine profiles in serum and peritoneal fluid from infertile women with and without endometriosis. J Obstet Gynaecol Res. 2007;33(4):490–495. Berbic M, Hey-Cunningham AJ, Ng C, et al. The role of Foxp3+ regulatory T-cells in endometriosis: a potential controlling mechanism for a complex, chronic immunological condition. Hum Reprod. 2010;25(4):900–907. Oosterlynck DJ, Meuleman C, Waer M, Koninckx PR, Vandeputte M. Immunosuppressive activity of peritoneal fluid in women with endometriosis. Obstet Gynecol. 1993;82(2):206–212. Kanzaki H, Wang HS, Kariya M, Mori T. Suppression of natural killer cell activity by sera from patients with endometriosis. Am J Obstet Gynecol. 1992;167(1):257–261. Ho HN, Wu MY, Yang YS. Peritoneal cellular immunity and endometriosis. Am J Reprod Immunol. 1997;38(6):400–412. Steinman RM. Decisions about dendritic cells: past, present, and future. Annu Rev Immunol. 2012;30:1–22. Steinman RM, Banchereau J. Taking dendritic cells into medicine. Nature. 2007;449(7161):419–426. Barton GM, Medzhitov R. Control of adaptive immune responses by Toll-like receptors. Curr Opin Immunol. 2002;14(3):380–383. Manicassamy S, Pulendran B. Dendritic cell control of tolerogenic responses. Immunol Rev. 2011;241(1):206–227. Schulke L, Berbic M, Manconi F, Tokushige N, Markham R, Fraser IS. Dendritic cell populations in the eutopic and ectopic endometrium of women with endometriosis. Hum Reprod. 2009;24(7):1695–1703. Na YJ, Jin JO, Lee MS, Song MG, Lee KS, Kwak JY. Peritoneal fluid from endometriosis patients switches differentiation of monocytes from dendritic cells to macrophages. J Reprod Immunol. 2008;77(1):63–74. Bacci M, Capobianco A, Monno A, et al. Macrophages are alternatively activated in patients with endometriosis and required for growth and vascularization of lesions in a mouse model of disease. Am J Pathol. 2009;175(2):547–556. Jung S, Unutmaz D, Wong P, et al. In vivo depletion of CD11c+ dendritic cells abrogates priming of CD8+ T cells by exogenous cell-associated antigens. Immunity. 2002;17(2):211–220. Styer AK, Sullivan BT, Puder M, et al. Ablation of leptin signaling disrupts the establishment, development, and maintenance of endometriosis-like lesions in a murine model. Endocrinology. 2008;149(2):506–514. Zukerberg LR, DeBernardo RL, Kirley SD, et al. Loss of cables, a cyclin-dependent kinase regulatory protein, is associated with the development of endometrial hyperplasia and endometrial cancer. Cancer Res. 2004;64(1):202–208. Bezbradica JS, Stanic AK, Matsuki N, et al. Distinct roles of dendritic cells and B cells in Va14Ja18 natural T cell activation in vivo. J Immunol. 2005;174(8):4696–4705. Nowak NM, Fischer OM, Gust TC, Fuhrmann U, Habenicht UF, Schmidt A. Intraperitoneal inflammation decreases endometriosis in a mouse model. Hum Reprod. 2008;23(11):2466–2474. Kao LC, Germeyer A, Tulac S, et al. Expression profiling of endometrium from women with endometriosis reveals candidate genes for disease-based implantation failure and infertility. Endocrinology. 2003;144(7):2870–2881. Author information Authors and Affiliations Corresponding authors Rights and permissions About this article Cite this article Stanic, A.K., Kim, M., Styer, A.K. et al. Dendritic Cells Attenuate the Early Establishment of Endometriosis-Like Lesions in a Murine Model. Reprod. Sci. 21, 1228–1236 (2014). https://doi.org/10.1177/1933719114525267 Published: Issue date: DOI: https://doi.org/10.1177/1933719114525267

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

mesh:D004715endometriosis

MeSH descriptors

Dendritic Cells Dendritic Cells Disease Models, Animal Endometriosis Endometriosis Animals Cell Count Cell Count Dendritic Cells Endometriosis Female Humans Immunity, Cellular Immunity, Cellular Mice Mice, Inbred C57BL Mice, Transgenic Time Factors

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (31)

Cited by (38)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pubmed
last seen: 2026-05-13T22:18:35.150238+00:00
License: CC0 · commercial use OK