ArticleFrontiers in immunology2019
Medroxyprogesterone Acetate Decreases Th1, Th17, and Increases Th22 Responses via AHR Signaling Which Could Affect Susceptibility to Infections and Inflammatory Disease.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- Distinct immunomodulatory effects of synthetic progestins compared with natural progesterone in human immune cells.ImmunoHorizons · 2026Article
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- Purinergic and Energy Metabolism Disruption in Oxidative Stress-Mediated Immunotoxicity Induced by Aflatoxin BJournal of fungi (Basel, Switzerland) · 2026Article
- Molecular crosstalk between AHR, CYP1B1, and ITGAM in diabetic nephropathy: Integrated insights from bioinformatics and experimental validation.Biochemistry and biophysics reports · 2026Article
- Therapeutic Effect of Baicalin-Loaded Thermosensitive Liposomal Hydrogel in Autoimmune Uveitis.ACS omega · 2026Article
- Integrative multi-omics analysis identifies genetically supported druggable targets for inflammatory bowel disease.Journal, genetic engineering & biotechnology · 2025Article
- Therapeutic selection for abnormal uterine bleeding with ovulatory dysfunction: a cross-sectional study in Chinese women.Future science OA · 2025Article
- Blood and sputum microbiota composition in Afghan immigrants and Iranian subjects with pulmonary tuberculosis.Iranian journal of microbiology · 2024Article
- Role of the type 3 cytokines IL-17 and IL-22 in modulating metabolic dysfunction-associated steatotic liver disease.Frontiers in immunology · 2024Review
- Possible Participation of Adenine Nucleotide Translocase ANT1 in the Cytotoxic Action of Progestins, Glucocorticoids, and Diclofenac on Tumor Cells.Pharmaceutics · 2023Article
- Signaling pathways and targeted therapies for psoriasis.Signal transduction and targeted therapy · 2023Review
- CD4+ T-cell subsets in autoimmune hepatitis: A review.Hepatology communications · 2023Review
- The Effect of Progestins on Cytokine Production in the Peripheral Blood Mononuclear Cells of Menopausal Women and Their Luminol-Dependent Chemiluminescence.Molecules (Basel, Switzerland) · 2023Article
- Article
- The gut microbiome: A line of defense against tuberculosis development.Frontiers in cellular and infection microbiology · 2023Review
- Old drugs, new tricks: leveraging known compounds to disrupt coronavirus-induced cytokine storm.NPJ systems biology and applications · 2022Article
- Progesterone as an Anti-Inflammatory Drug and Immunomodulator: New Aspects in Hormonal Regulation of the Inflammation.Biomolecules · 2022Review
- Role of hormones in the pregnancy and sex-specific outcomes to infections with respiratory viruses.Immunological reviews · 2022Review
- Medroxyprogesterone Acetate for Abnormal Uterine Bleeding Due to Ovulatory Dysfunction: The Effect of 2 Different-Duration Regimens.Medical science monitor : international medical journal of experimental and clinical research · 2022Article
- Perimenstrual Asthma in Adolescents: A Shared Condition in Pediatric and Gynecological Endocrinology.Children (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A synthetic progestin, medroxyprogesterone acetate (MPA), was used in a novel study to determine progestin effects on human purified macrophages and Th1, Th2, Th17, Th22 cells. MPA concentrations were equivalent to those in the serum of women after 6 and 9 months of progestin use. MPA has no effect on the proliferation of PBMCs and CD4+ T cell clones induced by immobilized anti-CD3 antibodies or by antigen (streptokinase). However, MPA decreases production and mRNA expression of IL-5, IL-13, IFN-γ, T-bet, RORC, and IL-17A but increases production and mRNA expression of IL-22 by CD4+ Th22 cell clones and decreases IL-22 production by Th17 cells. MPA inhibits RORC, but not T-bet and AHR, by Th17 cells but increases AHR mRNA and T-bet expression of established CD4+ Th22 cell clones. This suggests that MPA, at concentrations equivalent to those found in the serum of women after treatment for contraception and hormone replacement therapy, can directly inhibit Th1 responses (against intracellular bacteria and viruses), Th17 (against extracellular bacteria and fungi), Th2 (against parasites) but MPA therapy increases IL-22 produced by Th22 cells mediated by an increased expression of AHR and T-bet controlling inflammation. MPA could be responsible for the tissue damage limited by IL-22 in absence of IL-17A.
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