The impact of reproductive hormones on T cell immunity; normal and assisted reproductive cycles

Alanazi, Hallah; Zhang, Yuan; Fatunbi, Joy; Luu, Than; Kwak-Kim, Joanne

doi:10.1016/j.jri.2024.104295

Cited by 4 publications

References 129 publications

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Regulator of G-Protein Signaling 2 Knockout in CD4+ T Cells Promotes Anti-Inflammatory T Cells, Enhancing Ovulation, and Oocyte Yield

Raff,

Benton,

Brummond

et al. 2024

Preprint

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Objective: To determine the downstream effects on ovarian function and immune cell differentiation in the ovary and uterus using a model in which RGS2 was knocked out specifically in CD4+ T cells. Design: Laboratory based experiments with female mice. Animals: Female congenic (fully backcrossed) and non-congenic (mixed strain) mice with CD4 T cell-specific RGS2 knockout. Exposure: Four-week-old female CD4 RGS2 knockout (CD4 RGS2KO) mice and their littermate controls (CD4 RGS2CTL) were subjected to superovulation using pregnant mare serum gonadotropins. Main Outcome Measures: Oocyte numbers, lymphocyte populations in the ovary and uterus, and serum estradiol and progesterone concentrations. Results: In non-congenic (mixed strain) mice, CD4 RGS2 knockout (KO) promoted higher oocyte ovulation and increased uterine total leukocyte numbers. Similarly, congenic (fully backcrossed strain) mice showed higher oocyte numbers and increased uterine total leukocytes in the CD4 RGS2KO mice compared to CD4 RGS2CTL mice. Pro-inflammatory CD4+ T helper (TH) 1 and TH17 cell frequencies in the ovary and uterus were unchanged, while Treg and TH2 cell frequencies were elevated, along with increased concentrations of estradiol and progesterone in the serum of CD4 RGS2KO mice. Conclusion: Our study highlights the important role of RGS2 in CD4+ T cells within the context of reproduction. The dysregulation of immune responses due to RGS2 knockout in CD4+ T cells appears to enhance oocyte production. Further research is warranted to elucidate the precise mechanisms by which RGS2 influences reproductive outcomes, including its impact on fecundability, endometrial receptivity, and successful implantation.

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Regulator of G-Protein Signaling 2 Knockout in CD4+ T Cells Promotes Anti-Inflammatory T Cells, Enhancing Ovulation, and Oocyte Yield

Raff,

Benton,

Brummond

et al. 2024

Preprint

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What immunology has to say about pesticide safety

Friedrich,

Zwirner

2024

Front. Immunol.

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The use of pesticides has enabled the development of contemporary industrial agriculture and significantly increased crop yields. However, they are also considered a source of environmental pollution and a potential hazard to human health. Despite national agencies and the scientific community analyzing pesticide safety, immunotoxicity assays are often not required, poorly designed, or underestimated. Epidemiological evidence indicates that pesticide exposure increases the risk of developing cancer. Therefore, pesticides may not only act as carcinogens per se but also as immunosuppressive agents that create a permissive context for tumor development. Given recent evidence demonstrating the critical role of the immune response in cancer progression, we will highlight the necessity of assessing the potential impacts of pesticides on the immune response, particularly on tumor immunosurveillance. In this Perspective article, we will focus on the need to critically review fundamental aspects of toxicological studies conducted on pesticides to provide a clearer understanding of the risks associated with exposure to these compounds to human health.

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Advances in research on malignant transformation of endometriosis-associated ovarian cancer

Chen,

Zhu,

2024

Front. Oncol.

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Endometriosis (EMs) is a prevalent chronic gynecological condition that depends on estrogen, marked by the presence of active endometrial tissue (glands and stroma) outside the uterus. Although pathologically benign, it exhibits biological behaviors such as invasion and metastasis akin to malignant tumors. Endometriosis-associated ovarian carcinoma (EAOC), arising from malignant transformation of EMs, poses significant clinical challenges. However, the mechanisms underlying EAOC pathogenesis remain incompletely understood, with a lack of reliable biomarkers for early diagnosis and personalized treatment strategies. Considering the significant number of EMs patients and the extended period during which malignant transformation can occur, EAOC deserves significant attention. Current research both domestically and internationally indicates that the pathogenesis of EAOC is complex, involving genetic mutations, immune microenvironment, oxidative stress, epigenetic changes, and related areas. This review summarizes the mechanisms underlying the development of EAOC.

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The impact of reproductive hormones on T cell immunity; normal and assisted reproductive cycles

Cited by 4 publications

References 129 publications

Regulator of G-Protein Signaling 2 Knockout in CD4+ T Cells Promotes Anti-Inflammatory T Cells, Enhancing Ovulation, and Oocyte Yield

Regulator of G-Protein Signaling 2 Knockout in CD4+ T Cells Promotes Anti-Inflammatory T Cells, Enhancing Ovulation, and Oocyte Yield

What immunology has to say about pesticide safety

Advances in research on malignant transformation of endometriosis-associated ovarian cancer

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