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Lawrence M. Nelson - One of the best experts on this subject based on the ideXlab platform.
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Autoimmune Oophoritis with Multiple Molecular Targets Mitigated by Transgenic Expression of Mater
Endocrinology, 2011Co-Authors: Noriyuki Otsuka, Zhi-bin Tong, Konstantina Vanevski, Mickie H. Cheng, Lawrence M. NelsonAbstract:Primary ovarian insufficiency (POI) resulting from ovarian autoimmunity is a poorly understood clinical condition lacking in effective treatments. Understanding the targets of the autoimmune response and induction of ovarian-specific tolerance would allow development of focused therapies to preserve fertility in an at-risk population. MATER (maternal antigen that embryos require) is a known ovarian autoantigen targeted in autoimmune syndromes of POI. We attempt to induce ovarian-specific tolerance via transgenic expression of the MATER antigen on potentially tolerogenic antigen-presenting cells (APC), which typically present antigen via the major histocompatibility complex (MHC) class II molecule. We hypothesize that expression of MATER in a MHC class II-dependent manner on APC can mediate induction of ovarian tolerance. We utilized a well-characterized murine model of ovarian autoimmunity, whereby Oophoritis develops after d 3 neonatal thymectomy (NTx). Wild-type and transgenic mice, carrying an MHC Class II-driven Mater gene (IE-Mater), were subjected to NTx and assessed for evidence of autoimmune Oophoritis. After disease induction by NTx, female mice carrying the IE-Mater transgene had significant reductions in histological Oophoritis (56%) and circulating ovarian autoantibodies (28%) compared with wild-type females (94% and 82%, respectively). Incidence of other autoimmunity was unaffected as assessed by antinuclear autoantibodies. Transgenic expression of MATER in APC can induce antigen-specific tolerance with a significant reduction in ovarian autoimmunity. Lack of complete disease protection suggests that other antigens may also play a role in autoimmune Oophoritis. As a known autoantigen in the human APS1 (autoimmune polyglandular syndrome type 1), which is associated with POI, MATER may represent a relevant target for future diagnostic and therapeutic clinical interventions.
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Autoimmune Oophoritis as a mechanism of follicular dysfunction in women with 46,XX spontaneous premature ovarian failure
Fertility and sterility, 2005Co-Authors: Vladimir K. Bakalov, J N Anasti, Karim A. Calis, Vien H. Vanderhoof, Ahalya Premkumar, Shu Chen, Jadwiga Furmaniak, B. Rees Smith, Maria J. Merino, Lawrence M. NelsonAbstract:Objective To assess the association between serum adrenal cortex autoantibodies and histologically confirmed autoimmune lymphocytic Oophoritis. Design Controlled, prospective. Setting Tertiary research center. Patient(s) Two hundred sixty-six women with 46,XX spontaneous premature ovarian failure. Intervention(s) Ovarian biopsy in 10 women. Main Outcome Measure(s) Serum adrenal cortex autoantibodies assessed by indirect immunofluorescence and autoimmune Oophoritis assessed by immunohistochemical lymphocyte markers. Result(s) We obtained a histologic diagnosis of autoimmune Oophoritis in four women who tested positive for adrenal cortex autoantibodies and excluded this diagnosis in ovarian biopsies from six women who tested negative for adrenal cortex autoantibodies (4/4 vs. 0/6). Women with histologically confirmed autoimmune Oophoritis had a greater total ovarian volume as assessed by transvaginal sonography (11.4 ± 5.6 mL vs. 1.5 ± 0.4 mL) (mean ± SEM). They were also more likely to have subclinical adrenal insufficiency and clinical signs of androgen deficiency (3/4 vs. 0/6). Overall, 10/266 women tested positive for adrenal cortex autoantibodies (3.8%, 95% confidence interval: 1.8%–6.5%). Conclusion(s) In women who present with 46,XX spontaneous premature ovarian failure as their primary concern there is a clear association between serum adrenal cortex autoantibodies and the presence of histologically confirmed autoimmune Oophoritis.
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Murine postthymectomy autoimmune Oophoritis develops in association with a persistent neonatal-like Th2 response.
Clinical immunology and immunopathology, 1997Co-Authors: Rita Maity, Rachel R. Caspi, Sharmila Nair, Luiz Vicente Rizzo, Lawrence M. NelsonAbstract:Abstract Autoimmune Oophoritis develops in some patients despite evidence of impaired cellular immunity. Here, using the murine postthymectomy model of autoimmune Oophoritis, we investigate the hypothesis that neonatal thymectomy induces autoimmune Oophoritis by disrupting the normal postnatal balance of T helper cell regulation. Stimulated CD4 + splenic lymphocytes from adult mice sham-operated as neonates produced the expected T helper type 1 (Th1) predominant response normally seen in adult mice (low levels of interleukin-4 and high levels of interferon gamma). In contrast, cells from adult mice thymectomized as neonates produced an inappropriate neonatal-like Th2-predominant response (high levels of interleukin-4 and low levels of interferon-gamma). Manipulations that restored the postnatal shift to an adult Th1-dominant pattern ameliorated the autoimmune Oophoritis. Thus, neonatal thymectomy abrogates the postnatal shift to a Th1-dominant pattern, and the resulting persistent neonatal-like Th2-dominant response is tightly associated with the development of postthymectomy autoimmune Oophoritis. These results (i) suggest that the postnatal shift to the normal adult Th1/Th2 balance is established by a thymus-dependent process and (ii) raise the possibility that specific genetic defects, as yet to be determined, might mimic the effect of neonatal thymectomy in this model, impair the development of normal Th1/Th2 balance, and be a cause autoimmunity. These results hold implications for the pathogenesis and possibly for the therapy of autoimmune polyglandular failure in humans.
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Post-thymectomy murine experimental autoimmune Oophoritis is associated with reduced natural killer cell activity
American journal of reproductive immunology (New York N.Y. : 1989), 1997Co-Authors: Rita Maity, Lawrence M. Nelson, Sharmila Nair, Rachel R. CaspiAbstract:PROBLEM: Natural killer (NK) cells can influence the immune response by secreting potent lymphokines. It has been suggested that NK cells have a suppressive action on B cells, and that impaired NK cell activity may play a role in some types of autoimmunity. NK cell abnormalities have been reported in women with premature ovarian failure. We therefore examined NK cell activity during the development of murine experimental autoimmune Oophoritis, which serves as a model for autoimmune ovarian failure in women. METHOD OF STUDY: Neonatally thymectomized and sham-operated C57B1/6 × A/J (B6A) mice were prepared and sacrificed at 4, 6, 8, and 10 weeks after surgery. Splenic NK cell activity was determined in groups of five or more mice by measuring the percent specific lysis of target YAC-1 lymphoma cells using a standard 4-hr chromium release cytotoxicity assay. The number of splenic NK cells in neonatally thymectomized and sham-operated animals was also compared using flow cytometry. In a subsequent experiment, interleukin 12 (IL-12; NK cell-stimulating factor) was administered to neonatal mice before neonatal thymectomy. RESULTS: Neonatally thymectomized mice with associated autoimmune Oophoritis had a 75% reduction in the number of splenic NK cells, and 50% or greater reduction in splenic NK cell activity at 4, 6, and 8 weeks after surgery. IL-12 treatment before neonatal thymectomy maintained NK cell activity and was shown to ameliorate the associated autoimmune Oophoritis. CONCLUSION: Murine post-thymectomy autoimmune Oophoritis is associated with reduced NK cell number and impaired NK cell activity, and in these respects the model is similar to premature ovarian failure in women. Research to define the relationship between NK cell abnormalities and the mechanism of ovarian failure in this model might lend insight into the pathogenesis of premature ovarian failure in women.
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Susceptibility to murine experimental autoimmune Oophoritis is associated with genes outside the major histocompatibility complex (MHC)
1996Co-Authors: Sharmila Nair, Rachel R. Caspi, Lawrence M. NelsonAbstract:PROBLEM : Neonatal thymectomy induces experimental autoimmune Oophoritis in certain strains of mice, and this serves as a model for human autoimmune Oophoritis. Because strong MHC associations have been noted in human autoimmune conditions, we investigated the role of MHC in determining susceptibility to murine experimental autoimmune Oophoritis. Strain A mice are highly susceptible to post-thymectomy autoimmunity, whereas strain B10 mice are relatively resistant. The availability of congenic strains of mice makes it possible to separate the effects of genetic background and specific H-2 haplotype. METHODS : We neonatally thymectomized A and B10 background female mice, and their H-2 congenic counterparts, and then evaluated the resulting ovarian disease at age 6 weeks. RESULTS : A.By mice, which have the A background and the H-2 b haplotype, developed severe disease equivalent to strain A mice. Similarly, B10.A mice, which have the B background and the H-2 a haplotype, failed to develop disease. Thus, H-2 a haplotype did not convey disease susceptibility. CONCLUSIONS : Our findings suggest that immune-regulatory regions outside the H-2 locus play an important role in determining susceptibility to murine post-thymectomy autoimmune Oophoritis. This is in accord with our previous findings in women that showed no association between MHC and premature ovarian failure. Thus, in this respect this model is similar to human autoimmune ovarian failure. This suggests that the non-MHC genes conveying susceptibility to autoimmune Oophoritis in mice might represent similar predisposing genes for premature ovarian failure in women.
Kenneth S. K. Tung - One of the best experts on this subject based on the ideXlab platform.
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Autoimmune Ovarian Inflammation Triggered by Proinflammatory (Th1) T Cells Is Compatible with Normal Ovarian Function in Mice1
2016Co-Authors: Ken Kasai, An Ming Luo, Kenneth S. K. TungAbstract:The detection of noninfectious ovarian inflammation (oopho-ritis) and serum ovarian autoantibodies in a patient with pre-mature ovarian failure is indicative of an autoimmune etiology. The mechanisms of autoimmune ovarian injury leading to loss of function are currently unknown. In this study we investigated the impact of Oophoritis on ovarian function based on two mu-rine autoimmune ovarian disease (AOD) models. AOD can be induced by thymectomy at Day 3 after birth (d3tx). D3tx mice develop ovarian inflammation and atrophy with loss of oocytes. In these mice, ovarian atrophy and not Oophoritis correlated with abnormal estrous cyclicity. The second AOD model is in-duced by active immunization of adult mice with a murine ZP3 peptide (pZP3) in adjuvant. After active immunization, the zona pellucida antibody titer, not Oophoritis, correlated with reduced fertility. To investigate the effect of Oophoritis in the absence of antibody response or ovarian atrophy, pZP3-specific T cells were passively transferred into naive syngeneic mice. This recruited cytokine-producing cells into the ovaries so that elevated cyto-kine production and its effect on ovarian function could be ex-amined. Recipients of pZP3-specific T cells developed severe granulomatous Oophoritis, and the diseased ovaries had elevated ovarian mRNA levels of interferon-g, interleukin-1b, and tumor necrosis factor a. Despite these changes, fertility rates and go-nadotropin-induced follicular development remained essentially normal. Therefore, normal ovarian function is compatible with severe ovarian inflammation mediated by autoreactive T cells
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autoimmune orchitis and autoimmune Oophoritis
The Autoimmune Diseases (Fifth Edition), 2014Co-Authors: Livia Lustig, Claudia Rival, Kenneth S. K. TungAbstract:Abstract Autoimmune diseases of the testis [experimental autoimmune orchitis (EAO)] and the ovary [autoimmune ovarian disease (AOD)] are causal to infertility. Sperm autoimmunity also occurs in vasectomized men. In addition, autoantigens expressed in the testis and ovary can express ectopically in numerous human cancers. As cancer/testis antigens, they are subjected to tolerogenic regulation as sperm antigens in normal subjects and confer negative influence on cancer immunity. Alternatively, some cancer/testis antigens (CTA) are highly immunogenic and are desirable as candidate antigens in human cancer vaccines. Study on the spontaneous models of EAO and AOD indicates that regulatory T cell (Treg) is critical in systemic tolerance of the testis and ovarian autoantigens. We discovered two distinct types of sperm autoantigens: one is not hidden and is protected by Treg and the other that is hidden and not protected by Treg. This invalidated the prevailing paradigm of complete testis antigen sequestration. AOD model induced by a novel pZP3 that discovered molecular mimicry at T-cell epitope, epitope spreading as a mechanism of autoantibody response, the retargeting of T cell–mediated injury from one anatomical target to another by autoantibody, and the novel neonatal ovarian autoimmune disease (nAOD) induced by maternal autoantibody in the first 5 days of life. The unique nAOD is a model of human autoimmune disease elicited by maternal autoantibodies including congenital heart block in newborn of lupus mothers with Ro/SSA autoantibodies. nAOD requires neonatal natural killer (NK) cells deficient in inhibitory receptor LY49i. Treg also controls nAOD development. Finally, Th1 CD4 response occurs that adoptively transfer nAOD. The most well-defined clinical autoimmune ovarian and testicular diseases are found in the rare monogenic autoimmune polyendocrine syndrome associated with autoimmune regulator mutations. Contrary to numerous experimental models, the episodic clinical human testis and ovarian autoimmune diseases remain incompletely defined.
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Induction and Immunohistology of Autoimmune Ovarian Disease in Cynomolgus Macaques (Macaca fascicularis)
American Journal of Pathology, 2010Co-Authors: Harini Bagavant, Colin Sharp, Barbara E. Kurth, Kenneth S. K. TungAbstract:Autoimmune ovarian disease (AOD) is a probable cause of human premature ovarian failure, and a potential complication of contraceptive vaccines based on ovarian antigens. The diagnosis depends on detection of noninfectious ovarian inflammation (Oophoritis) and serum antibody to ovarian and placental antigens. Mechanisms underlying AOD have been investigated in mice but not in primates. Herein, we report induction of AOD in primates, and compare the immunopathology between monkey and murine AOD. Four cynomolgus macaques immunized with monkey or human zona pellucida 3 peptide (pZP3) in adjuvant, developed T-cell responses to the immunizing peptide and produced antibody that bound to native zona pellucida in vivo. Immunostaining of ovaries from pZP3-immunized macaques showed numerous clusters of T cells co-localized with major histocompatibility complex II-positive macrophages in the ovarian interstitium. Such foci were not detected in untreated or adjuvant-treated control monkeys. This finding is comparable to murine pZP3-induced AOD. However, unlike murine AOD in which numerous granulomatous lesions are detected, severe granulomatous inflammation was detected in only one of three monkeys with abnormal immunohistology. Similar to mice with pZP3-induced AOD, the immunized monkeys retained normal ovarian function. The results are discussed in the context of complications of ZP-based human immunocontraceptive vaccines and case reports of human autoimmune Oophoritis.
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The relative contribution of the CD28 and gp39 costimulatory pathways in the clonal expansion and pathogenic acquisition of self-reactive T cells.
Journal of Experimental Medicine, 1996Co-Authors: Nathan D. Griggs, Sally S. Agersborg, Randolf J. Noelle, Jeffrey A. Ledbetter, Peter S. Linsley, Kenneth S. K. TungAbstract:The zona pellucida (ZP), an ovarian extracellular structure, contains three major glycoproteins: ZP1, ZP2, and ZP3. A ZP3 peptide contains both an autoimmune Oophoritis-inducing T cell epitope and a B cell epitope that induces autoantibody to ZP. This study investigates two major T cell costimulation pathways in this disease model. Herein we show that blockage of glycoprotein (gp)39 and CD40 interaction with gp39 monoclonal antibody (mAb) results in the failure to induce both autoimmune Oophoritis and autoantibody production. Inhibition of ligand binding to the CD28 receptor with the fusion protein, murine CTLA4-immunoglobulin (Ig), also results in failure to generate antibody to ZP and significantly reduces disease severity and prevalence. Surprisingly, the frequencies of antigen-specific T cells in anti-gp39 mAb-treated mice, CTLA4-Ig treated mice, and in mice given control hamster IgG or control fusion protein L6, were equivalent as determined by limiting dilution analysis (approximately equals 1:5,000). These T cells, which produced comparable amounts of interleukin 4 and interferon gamma in vitro, were able to transfer Oophoritis to normal recipients. When anti-gp39 mAb and CTLA4-Ig were given together, the effect was additive, leading to inhibition of T cell activation as determined by in vitro proliferation and limiting dilution analysis (approximately equals 1:190,000); disease and antibody responses were absent in these mice. By studying these two costimulatory pathways in parallel, we have shown that autoimmune disease and autoantibody production are inhibitable by blocking either the gp39 or the CD28 pathway, whereas inhibition of clonal expansion of the effector T cell population occurs only when both pathways are blocked.
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Altered target organ. A mechanism of postrecovery resistance to murine autoimmune Oophoritis.
Journal of immunology (Baltimore Md. : 1950), 1995Co-Authors: Yahuan Lou, Fairley Mcelveen, Sallie Adams, Kenneth S. K. TungAbstract:Experimental murine autoimmune Oophoritis, a model of human premature ovarian failure, is induced by immunization with a peptide of the ZP3 glycoprotein from mouse zona pellucida (ZP3(330-340)) in CFA. The ovarian pathology is mediated by ZP3-specific, CD4+ T cells, and not by Abs. We now show that mice recovered from autoimmune Oophoritis in 4 mo, as characterized by regression of ovarian inflammation. Recovery was associated with disease resistance upon rechallenge with ZP3(330-340) in CFA. Oophoritis resistance was not explicable by immunosuppressive effect of CFA priming, nor by suppression of pathogenic T cells. ZP3-specific, proliferative T cell response could be detected, and a ZP3-specific, IFN-gamma-producing pathogenic T cell line was derived readily from the recovered mice by in vitro stimulation with the ZP3(330-340) peptide. Moreover, recovered mice, when challenged with ZP3(330-340) in CFA, produced Abs of IgG class to the ZP3(330-340) peptide. Suppressor T cells are not readily demonstrable. Most importantly, Oophoritis occurred in normal ovaries implanted under the renal capsule of the recovered mice. That Oophoritis developed in the implanted ovaries, but spared the endogenous ovaries, further indicates that the latter is refractory to Oophoritis. Disease resistance of the ovaries is not explicable by limitation of accessible target Ags. When mated, recovered mice were fertile and produced normal litters; and, as recipients of a ZP3-specific T cell line, their ovaries developed Oophoritis. We conclude that altered local environment of the target organ following autoimmune disease recovery can contribute to the complex disease-resistant state.
N. Peter Libbey - One of the best experts on this subject based on the ideXlab platform.
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Xanthogranulomatous Salpingitis and Oophoritis
2009Co-Authors: Yulia Gray, N. Peter LibbeyAbstract:Abstract A case of xanthogranulomatous salpingitis and Oophoritis in a 47-year-old woman is presented. Xanthogranulomatous inflammation is an uncommon form of chronic inflammation that is destructive to affected organs; it is characterized by the presence of lipid-filled macrophages with admixed lymphocytes, plasma cells, and neutrophils. Only a few cases of xanthogranulomatous salpingitis and Oophoritis have been reported to date. The case presented here is associated with Escherichia coli infection, endometriosis, and an intrauterine device.
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Xanthogranulomatous salpingitis and Oophoritis: a case report and review of the literature.
Archives of pathology & laboratory medicine, 2001Co-Authors: Yulia Gray, N. Peter LibbeyAbstract:○ A case of xanthogranulomatous salpingitis and Oophoritis in a 47-year-old woman is presented. Xanthogranulomatous inflammation is an uncommon form of chronic inflammation that is destructive to affected organs; it is characterized by the presence of lipid-filled macrophages with admixed lymphocytes, plasma cells, and neutrophils. Only a few cases of xanthogranulomatous salpingitis and Oophoritis have been reported to date. The case presented here is associated with Escherichia coli infection, endometriosis, and an intrauterine device.
Sharmila Nair - One of the best experts on this subject based on the ideXlab platform.
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Murine postthymectomy autoimmune Oophoritis develops in association with a persistent neonatal-like Th2 response.
Clinical immunology and immunopathology, 1997Co-Authors: Rita Maity, Rachel R. Caspi, Sharmila Nair, Luiz Vicente Rizzo, Lawrence M. NelsonAbstract:Abstract Autoimmune Oophoritis develops in some patients despite evidence of impaired cellular immunity. Here, using the murine postthymectomy model of autoimmune Oophoritis, we investigate the hypothesis that neonatal thymectomy induces autoimmune Oophoritis by disrupting the normal postnatal balance of T helper cell regulation. Stimulated CD4 + splenic lymphocytes from adult mice sham-operated as neonates produced the expected T helper type 1 (Th1) predominant response normally seen in adult mice (low levels of interleukin-4 and high levels of interferon gamma). In contrast, cells from adult mice thymectomized as neonates produced an inappropriate neonatal-like Th2-predominant response (high levels of interleukin-4 and low levels of interferon-gamma). Manipulations that restored the postnatal shift to an adult Th1-dominant pattern ameliorated the autoimmune Oophoritis. Thus, neonatal thymectomy abrogates the postnatal shift to a Th1-dominant pattern, and the resulting persistent neonatal-like Th2-dominant response is tightly associated with the development of postthymectomy autoimmune Oophoritis. These results (i) suggest that the postnatal shift to the normal adult Th1/Th2 balance is established by a thymus-dependent process and (ii) raise the possibility that specific genetic defects, as yet to be determined, might mimic the effect of neonatal thymectomy in this model, impair the development of normal Th1/Th2 balance, and be a cause autoimmunity. These results hold implications for the pathogenesis and possibly for the therapy of autoimmune polyglandular failure in humans.
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Post-thymectomy murine experimental autoimmune Oophoritis is associated with reduced natural killer cell activity
American journal of reproductive immunology (New York N.Y. : 1989), 1997Co-Authors: Rita Maity, Lawrence M. Nelson, Sharmila Nair, Rachel R. CaspiAbstract:PROBLEM: Natural killer (NK) cells can influence the immune response by secreting potent lymphokines. It has been suggested that NK cells have a suppressive action on B cells, and that impaired NK cell activity may play a role in some types of autoimmunity. NK cell abnormalities have been reported in women with premature ovarian failure. We therefore examined NK cell activity during the development of murine experimental autoimmune Oophoritis, which serves as a model for autoimmune ovarian failure in women. METHOD OF STUDY: Neonatally thymectomized and sham-operated C57B1/6 × A/J (B6A) mice were prepared and sacrificed at 4, 6, 8, and 10 weeks after surgery. Splenic NK cell activity was determined in groups of five or more mice by measuring the percent specific lysis of target YAC-1 lymphoma cells using a standard 4-hr chromium release cytotoxicity assay. The number of splenic NK cells in neonatally thymectomized and sham-operated animals was also compared using flow cytometry. In a subsequent experiment, interleukin 12 (IL-12; NK cell-stimulating factor) was administered to neonatal mice before neonatal thymectomy. RESULTS: Neonatally thymectomized mice with associated autoimmune Oophoritis had a 75% reduction in the number of splenic NK cells, and 50% or greater reduction in splenic NK cell activity at 4, 6, and 8 weeks after surgery. IL-12 treatment before neonatal thymectomy maintained NK cell activity and was shown to ameliorate the associated autoimmune Oophoritis. CONCLUSION: Murine post-thymectomy autoimmune Oophoritis is associated with reduced NK cell number and impaired NK cell activity, and in these respects the model is similar to premature ovarian failure in women. Research to define the relationship between NK cell abnormalities and the mechanism of ovarian failure in this model might lend insight into the pathogenesis of premature ovarian failure in women.
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Susceptibility to murine experimental autoimmune Oophoritis is associated with genes outside the major histocompatibility complex (MHC)
1996Co-Authors: Sharmila Nair, Rachel R. Caspi, Lawrence M. NelsonAbstract:PROBLEM : Neonatal thymectomy induces experimental autoimmune Oophoritis in certain strains of mice, and this serves as a model for human autoimmune Oophoritis. Because strong MHC associations have been noted in human autoimmune conditions, we investigated the role of MHC in determining susceptibility to murine experimental autoimmune Oophoritis. Strain A mice are highly susceptible to post-thymectomy autoimmunity, whereas strain B10 mice are relatively resistant. The availability of congenic strains of mice makes it possible to separate the effects of genetic background and specific H-2 haplotype. METHODS : We neonatally thymectomized A and B10 background female mice, and their H-2 congenic counterparts, and then evaluated the resulting ovarian disease at age 6 weeks. RESULTS : A.By mice, which have the A background and the H-2 b haplotype, developed severe disease equivalent to strain A mice. Similarly, B10.A mice, which have the B background and the H-2 a haplotype, failed to develop disease. Thus, H-2 a haplotype did not convey disease susceptibility. CONCLUSIONS : Our findings suggest that immune-regulatory regions outside the H-2 locus play an important role in determining susceptibility to murine post-thymectomy autoimmune Oophoritis. This is in accord with our previous findings in women that showed no association between MHC and premature ovarian failure. Thus, in this respect this model is similar to human autoimmune ovarian failure. This suggests that the non-MHC genes conveying susceptibility to autoimmune Oophoritis in mice might represent similar predisposing genes for premature ovarian failure in women.
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Murine experimental autoimmune Oophoritis develops independently of gonadotropin stimulation and is primarily localized in the stroma and theca.
American journal of reproductive immunology (New York N.Y. : 1989), 1995Co-Authors: Sharmila Nair, George Mastorakos, Shailaja G. Raj, Lawrence M. NelsonAbstract:PROBLEM: Neonatal thymectomy performed on day 3 of life (NTX3) induces experimental autoimmune Oophoritis in certain strains of mice. The disease has its onset around the time of the first estrous, suggesting the process may be gonadotropin dependent. Furthermore, one study reported that gonadotropin stimulation exacerbated the ovarian lymphocytic infiltration in NTX3 mice. Here we examine the possibility that gonadotropin stimulation of the ovary plays a role in the development of post-thymectomy autoimmune Oophoritis. METHOD: Using immunohistochemistry we defined the time course and histologic distribution of the post-thymectomy ovarian lymphocytic infiltration that develops in B6A mice ([C57BL6 × A/J]F1). We detected ovarian leukocytes using a monoclonal antibody against mouse CD45/T200 and counted those positive staining cells that had the morphologic appearance of lymphocytes. We then treated NTX3 mice to determine if gonadotropin stimulation could exacerbate the disease or cause the disease to appear earlier. We also treated NTX3 mice to determine if gonadotropin suppression could reduce the severity of the disease. RESULTS: Ovarian lymphocytic infiltration was observed as early as 3 weeks after thymectomy, and, during the course of the disease, was primarily located in the stroma and theca. Gonadotropin stimulation did not exacerbate existing disease or induce an earlier onset of severe disease. Furthermore, gonadotropin suppression did not reduce the degree of lymphocytic infiltration or oocyte destruction. CONCLUSIONS: Our findings suggest that murine experimental autoimmune Oophoritis develops independently of gonadotropin stimulation of the ovary.
н к сіліна - One of the best experts on this subject based on the ideXlab platform.
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complicated chronic salpingo Oophoritis in young women possibilities of conservative therapy
Reproductive Endocrinology, 2020Co-Authors: л в калугіна, т і юско, е ф чайківська, к д плаксієва, н к сілінаAbstract:Purpose of the study: to improve the scheme of conservative treatment of chronic salpingo-Oophoritis complicated by hydrosalpinx in young women. Materials and methods. The study included 65 patients with chronic salpingo-Oophoritis complicated by hydrosalpinx. The mean age of patients was 28 ± 5.9 years. Women were randomized into 2 groups depending on the therapy scheme. Group I (33 women) in addition to the standard complex were prescribed Distreptaza® suppositories rectally for a period of 15 days. Group II (32 women) received a standard complex, which included an antibacterial drug and a symbiotic. The diagnostic complex carried out in the treatment dynamics included a general clinical, gynecological examination, microbiological studies. Ultrasound and determination of luteinizing hormone, follicle-stimulating hormone, prolactin, estradiol and progesterone in plasma were performed before therapy and 1 month after. Results. Faster regression of pain in patients receiving treatment with Distreptaza® was accompanied by no sonographic signs of distal occlusion in fallopian tube in 48.48% patients; standard therapy was effective in 21.87% women. Microbiocenosis of the genital tract was restored in most patients of the examined groups after a month of treatment. There was a significant (p <0.05) 3-fold increase in progesterone levels in the second phase of the menstrual cycle after the end of antibacterial therapy in the first group. This is indicated the resumption of ovulatory cycles. This is makes it appropriate to use the selected drugs combination in young patients (up to 35 years) with unrealized reproductive plans. Conclusions. Treatment of chronic salpingo-Oophoritis complicated by hydrosalpinx in young women should be comprehensive and include in the first stage empirical antibacterial, anti-inflammatory and antifungal therapy, symbiotics and polyenzyme drugs. Organ-preserving methods should be preferred among surgical methods№ 4
