Inhibition of Follicle-Stimulating Hormone Receptor Binding by CirculatingImmunoglobulins*

Chiauzzi, Violeta A.; Cigorraga, Selva Beatriz; Escobar, María Eugenia; Rivarola, Marco A.; Charreau, Eduardo H.

doi:10.1210/jcem-54-6-1221

Cited by 118 publications

(44 citation statements)

References 26 publications

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“…Such autoantibodies have been characterized as steroid cell Abs including Abs to P450-17␣-hydroxylase and its side chain cleavage product (7,44). Abs to FSH and LH hormones and to FSH and LH receptors have been reported in POF but only in a small number of patients (45)(46)(47)(48). Similarly, autoantibodies specific for ZP proteins occur in Ͻ2.5% of POF patients (49).…”

Section: Discussionmentioning

confidence: 99%

Autoimmune Targeted Disruption of the Pituitary-Ovarian Axis Causes Premature Ovarian Failure

Altuntas

Johnson

Tuohy

2006

The Journal of Immunology

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Premature ovarian failure (POF) is characterized by amenorrhea and high serum levels of follicle-stimulating hormone (FSH). POF causes female infertility and represents a substantial women’s health risk affecting 1% of women by age 40. Although ovarian autoimmunity has been associated with POF, the identity of ovarian Ags recognized is unknown. In this study, we show that autoimmune-targeted disruption of the pituitary-ovarian axis leads to POF. Immunization of SWXJ female mice with the p215–234 peptide derived from mouse inhibin-α activates CD4+ T cells and induces experimental autoimmune oophoritis with a unique biphasic phenotype characterized by an early stage of enhanced fertility followed by a delayed stage of POF. Affected mice show high serum levels of inhibin-α-neutralizing Abs that prevent inhibin-mediated down-regulation of activin-induced pituitary FSH release. The loss of activin/FSH down-regulation leads to prolonged metestrus-diestrus, superovulation, increased numbers of mature follicles, increased offspring, accelerated depletion of primordial follicles, and ultimately premature infertility. Thus, inhibin-α-targeted experimental autoimmune oophoritis is initiated by CD4+ Th1 T cells that stimulate B cells to produce inhibin-α-neutralizing Abs directly capable of mediating POF and transferring disease into naive recipients. Our inhibin-α autoimmune model of POF shows how premature infertility may develop in the context of elevated FSH levels thereby closely mimicking the hallmark features of human POF.

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Section: Discussionmentioning

confidence: 99%

Autoimmune Targeted Disruption of the Pituitary-Ovarian Axis Causes Premature Ovarian Failure

Altuntas

Johnson

Tuohy

2006

The Journal of Immunology

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“…In addition, an ovarian biopsy may reveal the absence of ovarian follicles or fibrotic ovaries with a few or numerous follicles, the latter being characteristic of the ovary resistant syndrome (Savage's syndrome) (6). The gonadotropin receptor blocking Abs have been reported to be involved in the ovary resistant syndrome (25); however, the presence of these has not yet been confirmed (26). Furthermore, in Ab-negative patients with POF an ovarian biopsy may be helpful in the diagnosis of rare cases of POF caused by granulomatous or infiltrative diseases (1).…”

Section: Discussionmentioning

confidence: 99%

Autoantibodies to steroidogenic enzymes in patients with premature ovarian failure with and without Addison's disease

Prà

Chen²,

Furmaniak³

et al. 2003

European Journal of Endocrinology

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Design: Adrenal cortex autoantibodies (ACA), steroid-producing cell autoantibodies (StCA) and autoantibodies (Abs) to steroidogenic enzymes in three groups of patients with premature ovarian failure (POF), 15 with autoimmune Addison's disease (AD), 26 with non-adrenal autoimmune diseases and 31 with isolated POF, have been assessed. Methods: ACA and StCA were measured using an immunofluorescence technique. Abs to 21-hydroxylase (21-OH), to 17a-hydroxylase (17a-OH) and to cytochrome P450 side-chain cleavage (P450scc) were measured using an immunoprecipitation assay. Results: Seventy-three percent of patients with POF and AD were positive for StCA, 93% for 17a-OH and/or P450scc Abs, 93% for ACA and 100% for 21-OH Abs. Among patients with POF and nonadrenal autoimmune diseases, 8% were positive for StCA, 12% for 17a-OH and/or P450scc Abs, and 8% and 12% for ACA and 21-OH Abs respectively. StCA, 17a-OH and/or P450scc Abs were all found in 10% of patients with isolated POF, and 13% had ACA and 21-OH Abs. All StCA-, 17a-OH-and/or P450scc Abs-positive patients were also positive for ACA and 21-OH Abs. Two patients with isolated POF who were ACA and 21-OH Ab positive developed AD 3 and 5 years after the onset of POF. Conclusion: This study has shown that, when POF is associated with AD, StCA, 17a-OH and/or P450scc Abs are present in the majority of patients, while in the other two groups these Abs are detectable in a much lower proportion of patients. Measurement of ACA/21-OH Abs in some patients with POF may be important in identifying patients at risk of developing overt AD.

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“…Follicle-stimulating hormone (FSH) receptor-blocking antibodies were first identified in 3 patients with myasthenia gravis complicated by amenorrhea due to gonadotropin-resistant ovary syndrome as documented by the presence of high levels of gonadotropin and numerous cortical primordial follicles at biopsy (120,121). A common immunological mechanism mediated by blocking antibodies to acetylcholine receptors and against FSH receptors was hypothesized in these two diseases.…”

Section: Pof Isolated or Associated With Autoimmune Diseases Other Thmentioning

confidence: 99%

Adrenal and ovarian autoimmunity

Betterle

Volpato²

1998

European Journal of Endocrinology

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Inhibition of Follicle-Stimulating Hormone Receptor Binding by CirculatingImmunoglobulins*

Cited by 118 publications

References 26 publications

Autoimmune Targeted Disruption of the Pituitary-Ovarian Axis Causes Premature Ovarian Failure

Autoimmune Targeted Disruption of the Pituitary-Ovarian Axis Causes Premature Ovarian Failure

Autoantibodies to steroidogenic enzymes in patients with premature ovarian failure with and without Addison's disease

Adrenal and ovarian autoimmunity

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