During process like local or systemic homeostatic disturbances due to infection, tissue injury, trauma or surgery, neoplastic growth or immunological disorders, the host responds with a defensive reaction, the acute phase response, which encompasses alterations in immune, metabolic, neuroendocrine functions. Beyond the triggering stimulus, innate immune cells, quickly manage to deal with such a threat and secrete proinflammatory cytokines like Tumour Necrosis Factor alpha (TNF-α), Interleukin 1 beta (IL-1β), and Interleukin 6 (IL-6). Beyond their immunological effects, these cytokines also activate the stress system within the central nervous system leading to the activation of the hypothalamic-pituitary-adrenal axis as an effectors arm. As such, the immune response mounted against pathogens is paralleled by a significantly altered hormonal response. In relation to the immunomodulatory influences of adrenal steroids, glucocorticoids (GCs) suppress the immune system at several levels, avoiding the possible adverse effects of an excessive immune response and helping to terminate it once the noxious stimulus was eliminated. Under some circumstances, particularly at the beginning of the immune response, GCs can also exert pro-inflammatory effects. But at high concentrations, GCs generally suppress immune and inflammatory responses arising during activation of innate and adaptive immune responses. As in many physiological processes, individual sensitivity to GCs is variable being determined by genetic and acquired factors. This kind of versatility of GCs effects, that also extends to immune cells, may be due to a series of mechanisms, including a familiar resistance linked to inactivating mutations of GR or SNP -Single Nucleotide Polymorphism- functions affecting transcription. In this context, we will conduct a Scoping Review (ScR) of the literature about SNPs in the glucocorticoid receptor gene (NR3C1). The general aim of this ScR is to examine the extent and nature of available evidence on chronic illnesses associated with SNPs in the glucocorticoid receptor gene. The scoping review will assess evidence from all observational study designs. We will conduct a search in MEDLINE and LILACS. No language restriction will be applied. We will also search The Cochrane Library, and Epistemonikos to identify systematic reviews as an additional mechanism to identify primary studies. These searches will aim to identify all articles related to SNPs in the GR gene and will not be restricted to those evaluating specific conditions. These searches will be supplemented by scanning references of relevant retrieved articles to identify any additional relevant studies. References will be screen by titles and abstracts, remaining potentially relevant articles will be screen as full texts. Two reviewers will independently screen all identified records for relevance. Conflicts between reviewers will be solved by consensus or by the lead systematic reviewer in consultation with the content experts, if required. We will create a diagram to show the number of studies in each population condition. One reviewer will chart the data using pre-tested data-charting forms. This data charting will be double-checked for accuracy by a second reviewer. We will resolve any disagreements about data extraction by referring to the study report and through discussion. Once data is charted for all included studies, we will tabulate the data for each new condition identified. Findings from the scoping reviews will be reported according to the newly developed, PRISMA for Scoping Reviews (PRISMA-ScR). When interpreting the review findings, we will make sure that the limitations of different study designs are carefully considered, though no quality assessment will be performed.

中文翻译：

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慢性疾病中糖皮质激素受体基因（NR3C1）的多态性：范围审查的协议。

在过程中，例如由于感染，组织损伤，创伤或手术，肿瘤生长或免疫学疾病引起的局部或全身体内稳态紊乱，宿主会以防御反应（急性期反应）作出反应，包括免疫，代谢，神经内分泌功能的改变。除了触发刺激之外，先天免疫细胞还可以迅速应对这种威胁并分泌促炎性细胞因子，例如肿瘤坏死因子α（TNF-α），白介素1 beta（IL-1β）和白介素6（IL-6）。除了其免疫学作用外，这些细胞因子还激活中枢神经系统内的应激系统，导致下丘脑-垂体-肾上腺轴作为效应器臂被激活。因此，对病原体的免疫反应与荷尔蒙反应显着改变平行。关于肾上腺类固醇的免疫调节作用，糖皮质激素（GCs）在多个水平上抑制了免疫系统，避免了过度免疫反应的可能不利影响，并在消除了有害刺激后帮助终止了免疫反应。在某些情况下，尤其是在免疫反应开始时，GC也会发挥促炎作用。但是在高浓度下，GC通常会抑制先天性和适应性免疫反应激活过程中产生的免疫和炎症反应。与许多生理过程一样，个体对GC的敏感性是由遗传因素和获得性因素决定的。这种GC效应的多功能性，还延伸到免疫细胞的原因可能是由于一系列机制，包括与GR或SNP的失活突变相关的常见抗性-单核苷酸多态性-影响转录的功能。在这种情况下，我们将对糖皮质激素受体基因（NR3C1）中的SNP进行文献研究。该ScR的总体目标是检查糖皮质激素受体基因中与SNP相关的慢性疾病的现有证据的程度和性质。范围评估将评估所有观察性研究设计的证据。我们将在MEDLINE和LILACS中进行搜索。没有语言限制。我们还将搜索Cochrane图书馆和Epistemonikos，以识别系统评价，作为识别基础研究的附加机制。这些搜索旨在确定与GR基因中SNP相关的所有文章，而不仅限于评估特定条件的文章。这些搜索将通过扫描相关检索文章的参考文献来补充，以识别任何其他相关研究。参考文献将按标题和摘要进行筛选，其余可能相关的文章将按全文显示。两名审阅者将独立筛选所有已识别记录的相关性。审阅者之间的冲突将通过共识解决，或者由首席系统审阅者与内容专家协商解决（如果需要）。我们将创建一个图表以显示每种人口状况下的研究数量。一位审阅者将使用预先测试的数据图表来绘制数据图表。第二位审阅者将仔细检查此数据图表的准确性。我们将通过参考研究报告并通过讨论来解决有关数据提取的任何分歧。一旦为所有纳入研究绘制了数据图表，我们将为每种确定的新病状列出数据。根据新开发的PRISMA范围审查（PRISMA-ScR），将报告范围审查的结果。在解释评价结果时，我们将确保仔细考虑不同研究设计的局限性，尽管不会进行质量评估。根据最新开发的PRISMA界定范围审查（PRISMA-ScR），将报告范围审查的发现。在解释评价结果时，我们将确保仔细考虑不同研究设计的局限性，尽管不会进行质量评估。根据最新开发的PRISMA界定范围审查（PRISMA-ScR），将报告范围审查的发现。在解释评价结果时，我们将确保仔细考虑不同研究设计的局限性，尽管不会进行质量评估。