A Mouse Gene Encoding an Oocyte Antigen Associated with Autoimmune Premature Ovarian Failure

Tong, Zhi-Bin

doi:10.1210/en.140.8.3720

Cited by 46 publications

(37 citation statements)

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“…[101][102][103] Intriguingly, the major antigenic target that has been identified is a maternaleffect gene essential for embryogenesis, NLRP5 (NACHT, LRR and PYD domains-containing protein 5, also called NALP5 or MATER). 104,105 Importantly, NLRP5, which is also highly restricted in its tissue distribution, is targeted as a parathyroid antigen in APS-1 patients, many of whom also displayed hypogonadism. 106 Whether the same autoantigen is targeted in Aire-deficient mice is uncertain, although in our hands, an antigen of the predicted size for murine NLRP5 (121 kD) was not detected.…”

Section: Aire Regulates Promiscuous Gene Expression In Mtecmentioning

confidence: 99%

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: Aire Regulates Promiscuous Gene Expression In Mtecmentioning

confidence: 99%

Ovarian autoimmune disease: clinical concepts and animal models

et al. 2014

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“…RNA concentration was quantified by absorbance at 260 nm. To perform RT-PCR, ϳ2 g of total RNA was reverse-transcribed into cDNAs with 1 g of oligo(dT) [12][13][14][15][16][17][18] using SuperScript Preamplication System (Life Technologies, Rockville, MD). To compare the expression of the mRNA of the oocyte 110-kDa Ag between samples, each sample was coamplified with hypoxanthine guanine phosphoribosyl transferase (HPRT) using PCR.…”

Section: Detection Of the 110-kda Oocyte Ag Messenger Rna By Rt-pcrmentioning

confidence: 99%

Endogenous Oocyte Antigens Are Required for Rapid Induction and Progression of Autoimmune Ovarian Disease Following Day-3 Thymectomy

Alard

Thompson

Agersborg

et al. 2001

The Journal of Immunology

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Female (C57BL/6×A/J)F1 mice undergoing thymectomy on day 3 after birth (d3tx) developed autoimmune ovarian disease (AOD) and autoimmune disease of the lacrimal gland. As both were prevented by normal adult CD25+ T cells, regulatory T cell depletion is responsible for d3tx diseases. AOD began as oophoritis at 3 wk. By 4 wk, AOD progressed to ovarian atrophy with autoantibody response against multiple oocyte Ag of early ontogeny. The requirement for immunogenic endogenous ovarian Ag was investigated in d3tx female mice, d3tx male mice, and d3tx neonatally ovariectomized (OX) females. At 8 wk, all mice had comparable lacrimalitis but only those with endogenous ovaries developed AOD in ovarian grafts. The duration of Ag exposure required to initiate AOD was evaluated in d3tx mice OX at 2, 3, or 4 wk and engrafted with an ovary at 4, 5, or 6 wk, respectively. The mice OX at 2 wk did not have oophoritis whereas ∼80% of mice OX at 3 or 4 wk had maximal AOD, thus Ag stimulus for 2.5 wk following d3tx is sufficient. AOD progression requires additional endogenous Ag stimulation from the ovarian graft. In mice OX at 3 wk, ovaries engrafted at 5 wk had more severe oophoritis than ovaries engrafted at 6 or 12 wk; moreover, only mice engrafted at 5 wk developed ovarian atrophy and oocyte autoantibodies. Similar results were obtained in mice OX at 4 wk. Thus endogenous tissue Ag are critical in autoimmune disease induction and progression that occur spontaneously upon regulatory T cell depletion.

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“…Mater, Floped, and Tle6 expression was observed in oocytes as early as the primary follicle stage [10,17,18]. Comparative studies showed the expression of the genes in several mammalian species, with a moderate degree of sequence conservation, suggesting the potential existence of the complex in all mammals (Table 1) [19][20][21][22].…”

Section: Role Of the Scmc In Meiotic Spindle Formation And Positioningmentioning

confidence: 99%

The subcortical maternal complex: multiple functions for one biological structure?

Bebbere

Masala

Albertini

et al. 2016

J Assist Reprod Genet

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The subcortical maternal complex (SCMC) is a multiprotein complex uniquely expressed in mammalian oocytes and early embryos, essential for zygote progression beyond the first embryonic cell divisions. Similiar to other factors encoded by maternal effect genes, the physiological role of SCMC remains unclear, although recent evidence has provided important molecular insights into different possible functions. Its potential involvement in human fertility is attracting increasing attention; however, the complete story is far from being told. The present mini review provides an overview of recent findings related to the SCMC and discusses its potential physiological role/s with the aim of inspiring new directions for future research.

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A Mouse Gene Encoding an Oocyte Antigen Associated with Autoimmune Premature Ovarian Failure

Cited by 46 publications

References 0 publications

Ovarian autoimmune disease: clinical concepts and animal models

Ovarian autoimmune disease: clinical concepts and animal models

Endogenous Oocyte Antigens Are Required for Rapid Induction and Progression of Autoimmune Ovarian Disease Following Day-3 Thymectomy

The subcortical maternal complex: multiple functions for one biological structure?

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