Autoimmune oophoritis as a mechanism of follicular dysfunction in women with 46,XX spontaneous premature ovarian failure

Bakalov, Vladimir K.; Anasti, James N.; Calis, Karim A.; Vanderhoof, Vien H.; Premkumar, Ahalya; Chen, Shu; Furmaniak, Jadwiga; Smith, B. R.; Merino, María J.; Nelson, Lawrence M.

doi:10.1016/j.fertnstert.2005.04.060

Cited by 164 publications

(156 citation statements)

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“…19,20 Thus, the incidence of autoimmune POI that is associated with these autoantibodies is approximately 4%. 21 More than 80% of patients with autoimmune Addison's disease possess serum antibodies that recognize the adrenal cortex (adrenal cortex antibodies, ACAs). 22 All women identified to date with histological evidence of autoimmune oophoritis possess ACA; paradoxically, the major target of ACA, 21-hydroxylase (CYP21A2), [22][23][24] is not expressed in the ovary.…”

Section: Autoimmune Oophoritis As a Cause For Primary Ovarian Insuffimentioning

confidence: 99%

“…In addition to autoantibodies to CYP21A2, autoantibodies to two other steroidogenic enzymes, P450 side chain cleavage (CYP11A1) and 17a-hydroxylase (CYP17), which convert cholesterol to pregnenolone, and progesterone to 17-hydroxyprogesterone, respectively, are present. 21,[25][26][27] Since these latter enzymes, unlike CYP21A2, are expressed in the ovary, the presence of these antibodies may signify the actual autoimmune targets of the ovary. Antibodies targeting P450ssc and CYP17 are termed 'steroid cell' (SC) antibodies, since in addition to binding the adrenal cortex, they bind placental syncytiotrophoblast cells, Leydig cells of the testes, and theca and luteal cells of the ovary.…”

Section: Autoimmune Oophoritis As a Cause For Primary Ovarian Insuffimentioning

confidence: 99%

“…26,28,29 Although diagnostic markers of POI for use in the clinic have not been developed to date, adrenal cortex autoantibodies are predictive of autoimmune oophoritis. 21 Conversely, a patient presenting with POI who is found to possess SC autoantibodies should be closely monitored for emergent adrenal insufficiency because of its overlap with, and the life-threatening nature of, Addison's disease. 21 Pathology Grossly, 60% of patients with POI present with enlarged, multicystic ovaries, while 33% and 7% show normal or small ovarian size, respectively.…”

Section: Autoimmune Oophoritis As a Cause For Primary Ovarian Insuffimentioning

confidence: 99%

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Ovarian autoimmune disease: clinical concepts and animal models

et al. 2014

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The ovary is not an immunologically privileged organ, but a breakdown in tolerogenic mechanisms for ovary-specific antigens has disastrous consequences on fertility in women, and this is replicated in murine models of autoimmune disease. Isolated ovarian autoimmune disease is rare in women, likely due to the severity of the disease and the inability to transmit genetic information conferring the ovarian disease across generations. Nonetheless, autoimmune oophoritis is often observed in association with other autoimmune diseases, particularly autoimmune adrenal disease, and takes a toll on both society and individual health. Studies in mice have revealed at least two mechanisms that protect the ovary from autoimmune attack. These mechanisms include control of autoreactive T cells by thymus-derived regulatory T cells, as well as a role for the autoimmune regulator (AIRE), a transcriptional regulator that induces expression of tissue-restricted antigens in medullary thymic epithelial cells during development of T cells. Although the latter mechanism is incompletely defined, it is well established that failure of either results in autoimmune-mediated targeting and depletion of ovarian follicles. In this review, we will address the clinical features and consequences of autoimmune-mediated ovarian infertility in women, as well as the possible mechanisms of disease as revealed by animal models.

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Section: Autoimmune Oophoritis As a Cause For Primary Ovarian Insuffimentioning

confidence: 99%

Section: Autoimmune Oophoritis As a Cause For Primary Ovarian Insuffimentioning

confidence: 99%

Section: Autoimmune Oophoritis As a Cause For Primary Ovarian Insuffimentioning

confidence: 99%

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Ovarian autoimmune disease: clinical concepts and animal models

et al. 2014

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“…A study of 266 women with 46,XX spontaneous premature ovarian failure showed a clear association between histologically-confirmed autoimmune oophoritis and serum adrenal cortex antibodies [10]. Autoimmune oo-phoritis is characterized by mononuclear cell infiltration into the theca layer of antral follicles.…”

Section: Autoimmune Causesmentioning

confidence: 99%

“…Non-ovarian antibodies potentially mediating autoimmune damage in POI include: autoantibodies to steroid producing cells, 3β-hydroxysteroid dehydrogenase (3β-HSD) autoantibodies, antibodies against FSH and LH receptors, anti-thyroid antibodies, anti-parathyroid antibodies, autoantibodies to a zona pellucid 3 epitope, etc. [10,15]. Apart from autoantibodies, alteration of T-cell subsets and T-cell-mediated injury, decrease in number and activity of natural killer cells may also be responsible for autoimmune ovarian damage [39].…”

Section: Autoimmune Causesmentioning

confidence: 99%

An update on primary ovarian insufficiency

Jin

Huang

2012

Sci. China Life Sci.

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Primary ovarian insufficiency (POI) occurs in about 1% of female population under the age of 40, leading to reproductive problems, an earlier encounter with menopausal symptoms, and complicated diseases. There are three presumable mechanisms involved in the development of POI, namely apoptosis acceleration, follicular maturation blocking and premature follicle activation, through the following studied causes: (i) chromosomal abnormalities or gene mutations: mostly involve X chromosome, such as FMR1 premutation; more and more potentially causal genes have been screened recently; (ii) metabolic disorders such as classic galactosaemia and 17-OH deficiency; (iii) autoimmune mediated ovarian damage: observed alone or with some certain autoimmune disorders and syndromes; but the specificity and sensitivity of antibodies towards ovary are still questionable; (iv) iatrogenic: radiotherapy or chemotherapy used in cancer treatment, as well as pelvic surgery with potential threat to ovaries' blood supply can directly damage ovarian function; (v) virus infection such as HIV and mumps; (vi) toxins and other environmental/lifestyle factors: cigarette smoking, toxins (e.g., 4-vinylcyclohexene diepoxide), and other environmental factors are associated with the development of POI. The etiology of a majority of POI cases is not identified, and is believed to be multifactorial. Strategies to POI include hormone replacement and infertility treatment. Assisted conception with donated oocytes has been proven to achieve pregnancy in POI women. Embryo cryopreservation, ovarian tissue cryopreservation and oocyte cryopreservation have been used to preserve ovarian reserve in women undergoing cancer treatments. Primary ovarian insufficiency (POI), commonly referred to as premature ovarian failure (POF), is defined as the occurrence of amenorrhea (for 4 months or more) before the age of 40 in women, accompanied with an increase of serum FSH to menopausal level (usually over 40 IU L 1 , obtained at least 1 month apart), and estradiol levels less than 50 pg mL 1 (which indicate hypoestrogenism) [1]. Primary ovarian insufficiency is first brought to light by Fuller Albright in 1942, who emphasized that the end stage of ovarian function is the primary defect rather than abnormality in gonadotropin secretion [2], and avoided the discomforting and inaccurate stressing on "failure", like death-sentence for ovarian function and conception.Menopause is a destined phase of women, which is expected to occur at around the age of (50±4) years in US women [3]. The age of 40 is two standard deviations below this average [4]. With an incidence of 1% in women under the age of 40, and 0.1% in women under the age of 30 [5], POI renders patients estrogen deficiency and anovulation, resulting in vasomotor symptoms (hot flashes and night sweats), atrophic vaginitis, dyspareunia, primary or secondary amenorrhea, and infertility. 76% of POI cases developed after normal puberty and establishment of regular menses [6]. Some of such conditions occur after stopping...

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T_reg deficiency‐mediated T_H1 response causes human premature ovarian insufficiency through apoptosis and steroidogenesis dysfunction of granulosa cells

Zhang

et al. 2021

Clinical & Translational Med

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Autoimmune oophoritis as a mechanism of follicular dysfunction in women with 46,XX spontaneous premature ovarian failure

Cited by 164 publications

References 32 publications

Ovarian autoimmune disease: clinical concepts and animal models

Ovarian autoimmune disease: clinical concepts and animal models

An update on primary ovarian insufficiency

T_reg deficiency‐mediated T_H1 response causes human premature ovarian insufficiency through apoptosis and steroidogenesis dysfunction of granulosa cells

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Autoimmune oophoritis as a mechanism of follicular dysfunction in women with 46,XX spontaneous premature ovarian failure

Cited by 164 publications

References 32 publications

Ovarian autoimmune disease: clinical concepts and animal models

Ovarian autoimmune disease: clinical concepts and animal models

An update on primary ovarian insufficiency

Treg deficiency‐mediated TH1 response causes human premature ovarian insufficiency through apoptosis and steroidogenesis dysfunction of granulosa cells

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Product

Resources

About

T_reg deficiency‐mediated T_H1 response causes human premature ovarian insufficiency through apoptosis and steroidogenesis dysfunction of granulosa cells