Long-term programming of sex differences in immunity by prenatal exposure to stress
通过产前暴露于压力对免疫性别差异进行长期规划
基本信息
- 批准号:453860814
- 负责人:
- 金额:--
- 依托单位:
- 依托单位国家:德国
- 项目类别:Research Units
- 财政年份:
- 资助国家:德国
- 起止时间:
- 项目状态:未结题
- 来源:
- 关键词:
项目摘要
Prenatal adverse environments such as the exposure to stress can impair immunity later in life of the offspring. In this context, a significant sex bias in immune disorders has been observed. Steroid hormones such as glucocorticoids are pivotal mediators of fetal development. Excess levels of glucocorticoids elicited by prenatal stress can cause cellular damage in the fetus. We previously identified differentially higher glucocorticoid levels in female compared to male offspring following prenatal stress. Moreover, hematopoietic stem cells had a differentially altered epigenetic signature in prenatally stressed females compared to stressed males. This was accompanied by a skewed frequency of lineage-committed cells, i.e. an increase of CD8+ effector T cells. Future experiments are now needed to unearth the biological consequences of prenatal stress for sex-specific immunity throughout life. We hypothesize that prenatal glucocorticoid surges in response to stress differentially affect CD8+ T cell-dependent long-term immunity in male and female offspring. In turn, sex-specific immunity against e.g. pathogens or anti-tumor responses is dampened, which perpetuates the courses of immune diseases. We will test this hypothesis by comprehensively analyzing antigen-specificity, effector functions and epigenetic stability of CD8+ T cells in male and female offspring exposed to prenatal stress. We will also evaluate the interaction of CD8+ T cells with glucocorticoids and other steroid hormones such as testosterone. The functional role of CD8+ T cell will be assessed in immune diseases with a clear female (influenza infection) or male (tumor response) sex bias. Our expected insights will advance the understanding of long-term programming of immunity, whilst promoting the identification of distinct pathways underlying the developmental origin of sex differences in immunity.
出生前的不利环境,如暴露于压力下,会损害后代以后的免疫力。在这种情况下,在免疫疾病中观察到了显著的性别偏见。类固醇激素如糖皮质激素是胎儿发育的关键介质。产前压力引起的糖皮质激素水平过高会导致胎儿细胞损伤。我们以前发现差异较高的糖皮质激素水平的女性相比,男性后代产前压力。此外,造血干细胞有差异改变的表观遗传签名在产前强调女性相比,强调男性。这伴随着谱系定型细胞的偏斜频率,即CD8+效应T细胞的增加。现在需要进一步的实验来揭示产前压力对终生性特异性免疫的生物学后果。我们推测,产前糖皮质激素激增响应压力差异影响CD8+ T细胞依赖的长期免疫的男性和女性后代。反过来,针对例如病原体或抗肿瘤反应的性别特异性免疫力被抑制,这使免疫疾病的病程持续下去。我们将通过全面分析暴露于产前应激的男性和女性后代中CD 8 + T细胞的抗原特异性、效应器功能和表观遗传稳定性来验证这一假设。我们还将评估CD8+ T细胞与糖皮质激素和其他类固醇激素(如睾酮)的相互作用。将评估CD8+ T细胞在具有明显女性(流感感染)或男性(肿瘤反应)性别偏倚的免疫疾病中的功能作用。我们预期的见解将促进对免疫长期编程的理解,同时促进识别免疫性别差异发展起源的不同途径。
项目成果
期刊论文数量(0)
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Professorin Dr. Petra Clara Arck其他文献
Professorin Dr. Petra Clara Arck的其他文献
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{{ truncateString('Professorin Dr. Petra Clara Arck', 18)}}的其他基金
Towards improving pregnancy success rates: Understanding the functional role and memory development of CD4+ regulatory T cell subsets during first and second pregnancies.
提高妊娠成功率:了解 CD4 调节性 T 细胞亚群在第一次和第二次妊娠期间的功能作用和记忆发育。
- 批准号:
315517090 - 财政年份:2016
- 资助金额:
-- - 项目类别:
Research Grants
Prenatal stress challenge in mice: the role of vertically transmitted maternal glucocorticoids and immune cells in modulating offspring‘s immunity
小鼠产前应激挑战:垂直传播的母体糖皮质激素和免疫细胞在调节后代免疫力中的作用
- 批准号:
269321214 - 财政年份:2015
- 资助金额:
-- - 项目类别:
Clinical Research Units
Influenza during pregnancy: The emergence of highly virulent H1N1 influenza virus strains and consequences for maternal and offspring’s health
怀孕期间流感:高毒力 H1N1 流感病毒株的出现及其对孕产妇和后代健康的影响
- 批准号:
269120464 - 财政年份:2015
- 资助金额:
-- - 项目类别:
Clinical Research Units
Fetale Ursache immunologischer Erkrankungen: Einfluss von mütterlichem Mikrochimärismus während der Schwangerschaft und dessen Modulation durch Stressbelastung
免疫疾病的胎儿原因:妊娠期间母体微嵌合的影响及其应激调节
- 批准号:
192644356 - 财政年份:2011
- 资助金额:
-- - 项目类别:
Research Grants
Immune mediated depressive behaviour: causes, consequences and therapeutic opportunities
免疫介导的抑郁行为:原因、后果和治疗机会
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28996577 - 财政年份:2007
- 资助金额:
-- - 项目类别:
Research Grants
Haarwuchsstörungen durch Stress: Nachweis, pathophysiologische Grundlagen und neuropharmakologische Manipulation, GEM mit PA 345/11-2
压力引起的毛发生长障碍:证据、病理生理学基础和神经药理学操作,GEM with PA 345/11-2
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5374272 - 财政年份:2002
- 资助金额:
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