Reproductive endocrinology

Multiracial Cytokine Profiling Reveals Immune Dysregulation not Chronic Inflammation in Polycystic Ovary Syndrome

J Clin Endocrinol MetabPublished Retrospective cross-sectional study

Authors' conclusion

This study challenges the prevailing notion of PCOS as a disorder of chronic low-grade inflammation, suggesting instead that immune suppression and impaired angiogenic signaling may be factors in PCOS pathophysiology, especially in nonobese patients. Further research with larger sample sizes and inclusion of metabolic metrics is needed to confirm these findings before they can be applied in clinical practice.

Study context

Population
Premenopausal women aged 18 to 45 years, Black and White, presenting for evaluation of androgen excess at reproductive endocrinology clinics (University of Alabama at Birmingham; Cedars-Sinai Medical Center)
Participants
40 women
Exposure
Polycystic ovary syndrome (PCOS) vs controls
  • PCOSn = 20
  • Controlsn = 20reference
Outcome
Fasted follicular phase plasma concentrations of C-reactive protein and 96 circulating immune markers (incl. IL-6, TNF-α, IL-18), Milliplex Luminex xMAP assay
Methodological detailsrace, age and BMI matched, Androgen Excess Biorepository samples 1987–2010
  • Race, age and BMI matched
  • Androgen Excess Biorepository samples 1987–2010

Main finding

As reported in the abstract

Circulating immune markers
  • PCOS showed significantly lower levels of circulating immune markers
  • Growth factors (VEGF-A, platelet-derived growth factor), proinflammatory cytokines (IL-8, TNF-α, interferon-γ) and several chemokines reduced in PCOS, independent of race
  • PCOS vs Controls: P < 0.05

Observational data: associations, not effects.

Further findings

Differences between Black and White women

Only IL-18 and CXCL16 differed significantly between Black and White women

Original publication

Multiracial Cytokine Profiling Reveals Immune Dysregulation not Chronic Inflammation in Polycystic Ovary Syndrome. J Clin Endocrinol Metab. Published 22 September 2025. doi:10.1210/clinem/dgaf524

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