Murine Experimental Autoimmune Oophoritis Develops Independently of Gonadotropin Stimulation and is Primarily Localized in the Stroma and Theca

Nair, Sharmila; Mastorakos, George; Raj, Shailaja G.; Nelson, Lawrence M.

doi:10.1111/j.1600-0897.1995.tb00929.x

Cited by 9 publications

(3 citation statements)

References 13 publications

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“…3B) of age. Thus, immunological recognition of ovarian targets often appears to begin at an early stage, independently of gonadotropin stimulation of follicular growth and ovulation, which is consistent with findings in the neonatal thymectomy model of ovarian autoimmune disease [26,27]. The reason we did not observe 100% penetrance of the follicular destruction phenotype is not clear, but it is possible that immune effectors (antibodies or T cells) mediating follicular destruction simply had not yet developed in these apparently unaffected mice.…”

Section: Discussionsupporting

confidence: 87%

The Autoimmune Regulator Prevents Premature Reproductive Senescence in Female Mice1

Jasti

Warren

McGinnis

et al. 2012

Biology of Reproduction

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Loss-of-function mutations in the autoimmune regulator (AIRE) gene are responsible for autoimmune polyglandular syndrome type 1 (APS-1), which commonly manifests as infertility in women. AIRE is a transcriptional regulator that promotes expression of tissue-restricted antigens in the thymus, including antigens specific to the ovary. Thymic expression of ovarian genes under AIRE's control may be critical for preventing ovarian autoimmune disease. Because mice lacking Aire are an important APS-1 model, we examined the reproductive properties of female Aire-deficient (Aire(-/-)) mice. Female Aire(-/-) mice on the BALB/c background were examined for reproductive parameters, including fertility, litter sizes, and ovarian follicular reserves. Although delayed puberty was observed in Aire(-/-) mice, all mice entered puberty and exhibited mating behavior. Only 50% of Aire(-/-) females gave an initial litter, and only 16% were able to produce two litters. Ovarian histopathologic examination revealed that 83% of previously bred females lost all ovarian follicular reserves. Among virgin females, follicular depletion was observed in 25% by 8 wk, and by 20 wk, 50%-60% of mice lost all follicles. This was associated with elevated serum follicle-stimulating hormone level and ovarian infiltration of proliferating CD3+ T lymphocytes. Ovulation rates of 6-wk-old Aire(-/-) mice were reduced by 22%, but this difference was not statistically significant. Finally, transplantation experiments revealed that follicular loss depended on factors extrinsic to the ovary. These results suggest that immune-mediated ovarian follicular depletion is a mechanism of infertility in Aire(-/-) mice. The results have important implications in the pathogenesis of ovarian autoimmune disease in women.

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Section: Discussionsupporting

confidence: 87%

The Autoimmune Regulator Prevents Premature Reproductive Senescence in Female Mice1

Jasti

Warren

McGinnis

et al. 2012

Biology of Reproduction

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“…In animal studies using thymectomised neonatal mice AOA titres correlated with the degree and progression of oophoritis [ 40 , 41 ]. A decline in the AOA titres correlated with the decline in ovarian function.…”

Section: Anti-oocyte Autoantibodiesmentioning

confidence: 99%

Autoimmune premature ovarian failure

Komorowska

2016

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Premature ovarian failure (POF), also termed as primary ovarian insufficiency (POI), is a highly heterogenous condition affecting 0.5-3.0% of women in childbearing age. These young women comprise quite a formidable group with unique physical and psychological needs that require special attention. Premature ovarian senescence (POS) in all of its forms evolves insidiously as a basically asymptomatic process, leading to complete loss of ovarian function, and POI/POF diagnoses are currently made at relatively late stages. Well-known and well-documented risk factors exist, and the presence or suspicion of autoimmune disorder should be regarded as an important one. Premature ovarian failure is to some degree predictable in its occurrence and should be considered while encountering young women with loss of menstrual regularity, especially when there is a concomitant dysfunction in the immune system.

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“…Ñòèìóëÿö³ÿ ãîíàäîòðîï³íîì íå ï³äñèëþâàëà âaeå âèêëèêàíèé ïàòîëîã³÷íèé ïðîöåñ é íå ïðèçâîäèëà äî á³ëüø ðàííüîãî ïî÷àòêó ñàìî¿ õâîðîáè; ñóïðåñ³ÿ ãîíàäîòðîï³íó íå çìåíøóâàëà ñòóï³íü ë³ìôîöèòàðíî¿ ³íô³ëüòðàö³¿ é óøêîäaeåííÿ îîöèòà. Ðåçóëüòàòè äàþòü ï³äñòàâè ïðèïóñêàòè, ùî åêñïåðèìåíòàëüíèé àóòî-³ìóííèé îîôîðèò ó ìèøåé ðîçâèâàºòüñÿ íåçàëåaeíî â³ä ñòèìóëÿö³¿ ÿº÷íèêà ãîíàäî-òðîï³íîì [19]. Äîçà àíòèãåíà ïðè ââåäåíí³ ZP3 çìåíøóâàëà ñòóï³íü âèðàaeåíîñò³ îîôîðèòó ó ïîð³âíÿíí³ ç êîíòðîëüíîþ ãðóïîþ, íîðìàë³çóâàëà åñòðàëüíèé öèêë é çá³ëüøóâàëà ê³ëüê³ñòü CD4 + Ò-êë³òèí, ó òîé ÷àñ ÿê ê³ëüê³ñòü CD25 + T-êë³òèí çìåíøóâàëàñÿ, ³ñòîòíî çìåíøóâàâñÿ é òèòð àóòîàíòèò³ë [12,13].…”

Section: åêñïåðèìåíòàëüíèé àóòî³ìóííèé îîôîðèòunclassified

Autoimmune mechanisms of ovarian pathology

TIu¹,

Om²,

Tv³

et al. 2011

Fiziol Zh

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Àóòî³ìóíí³ ìåõàí³çìè ïàòîëîã³¿ ÿº÷íèê³â Â îãëÿä³ ïðåäñòàâëåí³ äàí³, ùî ñòîñóþòüñÿ àóòî³ìóííî¿ ïàòîëîã³¿ ÿº÷íèê³â ó ae³íîê. Ðîçãëÿäàþòüñÿ åêñïåðèìåíòàëüí³ ìîäåë³ àóòî³ìóííî¿ ïàòîëîã³¿ ÿº÷íèê³â ç âèêîðèñòàííÿì òâàðèí. Íàâîäÿòüñÿ ðåçóëüòàòè âëàñíèõ äîñë³äaeåíü åêñïåðèìåíòàëüíî¿ ³ìóííî¿ ïàòîëîã³¿ ÿº÷íèê³â ó ìèøåé. Êëþ÷îâ³ ñëîâà: àóòî³ìóííà ïàòîëîã³ÿ ÿº÷íèê³â, åêñïåðèìåíòàëüíèé àóòî³ìóííèé äèñãåíåç ÿº÷íèê³â, åêñïåðèìåíòàëüíèé àóòî³ìóííèé îîôîðèò, åêñïåðèìåíòàëüíà ³ìóííà ïàòîëîã³ÿ ÿº÷íèê³â.

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Murine Experimental Autoimmune Oophoritis Develops Independently of Gonadotropin Stimulation and is Primarily Localized in the Stroma and Theca

Abstract: Our findings suggest that murine experimental autoimmune oophoritis develops independently of gonadotropin stimulation of the ovary.

Cited by 9 publications

References 13 publications

The Autoimmune Regulator Prevents Premature Reproductive Senescence in Female Mice1

The Autoimmune Regulator Prevents Premature Reproductive Senescence in Female Mice1

Autoimmune premature ovarian failure

Autoimmune mechanisms of ovarian pathology

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