Polycystic ovary syndrome

Stener-Victorin, Elisabet; Teede, Helena; Norman, Robert J.; Legro, Richard; Goodarzi, Mark O.; Dokras, Anuja; Laven, Joop; Hoeger, Kathleen; Piltonen, Terhi T.

doi:10.1038/s41572-024-00511-3

Cited by 35 publications

(1 citation statement)

References 289 publications

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“…The immune system is linked to several features of polycystic ovary syndrome (PCOS), including reproductive complications and metabolic comorbidities. [ 1 ] Yet, it remains largely unknown how hyperandrogenism, a hallmark of PCOS, affects the immune system.…”

Section: Introductionmentioning

confidence: 99%

Androgens Modulate the Immune Profile in a Mouse Model of Polycystic Ovary Syndrome

Torstensson,

Ascani,

Risal

et al. 2024

Advanced Science

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Polycystic ovary syndrome (PCOS) is associated with a low‐grade inflammation, but it is unknown how hyperandrogenism, the hallmark of PCOS, affects the immune system. Using a PCOS‐like mouse model, it is demonstrated that hyperandrogenism affects immune cell populations in reproductive, metabolic, and immunological tissues differently in a site‐specific manner. Co‐treatment with an androgen receptor antagonist prevents most of these alterations, demonstrating that these effects are mediated through androgen receptor activation. Dihydrotestosterone (DHT)‐exposed mice displayed a drastically reduced eosinophil population in the uterus and visceral adipose tissue (VAT). A higher frequency of natural killer (NK) cells and elevated levels of IFN‐γ and TNF‐α are seen in uteri of androgen‐exposed mice, while NK cells in VAT and spleen displayed a higher expression level of CD69, a marker of activation or tissue residency. Distinct alterations of macrophages in the uterus, ovaries, and VAT are also found in DHT‐exposed mice and can potentially be linked to PCOS‐like traits of the model. Indeed, androgen‐exposed mice are insulin‐resistant, albeit unaltered fat mass. Collectively, it is demonstrated that hyperandrogenism causes tissue‐specific alterations of immune cells in reproductive organs and VAT, which can have considerable implications on tissue function and contribute to the reduced fertility and metabolic comorbidities associated with PCOS.

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Section: Introductionmentioning

confidence: 99%

Androgens Modulate the Immune Profile in a Mouse Model of Polycystic Ovary Syndrome

Torstensson,

Ascani,

Risal

et al. 2024

Advanced Science

Self Cite

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Addressing Polycystic Ovary Syndrome in Pregnancy Care to Improve Outcomes

Bahri Khomami,

Teede

2024

JAMA Netw Open

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What can we do for the adolescents with polycystic ovary syndrome?

Chen,

Tang,

et al. 2024

World J Pediatr

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Polycystic ovary syndrome (PCOS) is a major health issue for females, resulting in a substantial health and economic burden globally [1]. Its manifestations often occur throughout the lifespan, typically arising in childhood and evolving through adolescence into adulthood [2], affecting approximately 6.3% of adolescent girls [3]. The aetiology of PCOS is complex, with a heterogenous clinical presentation involving reproductive, metabolic, and psychological features [4]. Women worldwide often experience delayed diagnosis and dissatisfaction with care [4], issues that are even more pronounced during adolescence [5], impacting the assessment and management of affected girls (Fig. 1).

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Polycystic ovary syndrome

Cited by 35 publications

References 289 publications

Androgens Modulate the Immune Profile in a Mouse Model of Polycystic Ovary Syndrome

Androgens Modulate the Immune Profile in a Mouse Model of Polycystic Ovary Syndrome

Addressing Polycystic Ovary Syndrome in Pregnancy Care to Improve Outcomes

What can we do for the adolescents with polycystic ovary syndrome?

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