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本文引用的文献

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Intestinal methane production in obese individuals is associated with a higher body mass index.肥胖个体的肠道甲烷生成与较高的体重指数相关。
Gastroenterol Hepatol (N Y). 2012 Jan;8(1):22-8.
2
Therapeutic paradox in CNS tuberculosis.中枢神经系统结核病中的治疗悖论
J Pediatr Neurosci. 2009 Jul;4(2):133-4. doi: 10.4103/1817-1745.57331.
3
No evidence of altered alveolar macrophage polarization, but reduced expression of TLR2, in bronchoalveolar lavage cells in sarcoidosis.在结节病的支气管肺泡灌洗液细胞中,没有肺泡巨噬细胞极化改变的证据,但 TLR2 的表达减少。
Respir Res. 2010 Sep 2;11(1):121. doi: 10.1186/1465-9921-11-121.
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A ChIP-seq defined genome-wide map of vitamin D receptor binding: associations with disease and evolution.一项 ChIP-seq 定义的维生素 D 受体结合的全基因组图谱:与疾病和进化的关联。
Genome Res. 2010 Oct;20(10):1352-60. doi: 10.1101/gr.107920.110. Epub 2010 Aug 24.
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Association between Epstein-Barr virus infection and risk for development of pregnancy-associated breast cancer: joint effect with vitamin D?EB 病毒感染与妊娠相关性乳腺癌发病风险的关联:与维生素 D 的联合作用?
Eur J Cancer. 2011 Jan;47(1):116-20. doi: 10.1016/j.ejca.2010.07.006. Epub 2010 Aug 4.
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Proinflammatory T-cell responses to gut microbiota promote experimental autoimmune encephalomyelitis.肠道微生物群诱导的促炎 T 细胞应答促进实验性自身免疫性脑脊髓炎。
Proc Natl Acad Sci U S A. 2011 Mar 15;108 Suppl 1(Suppl 1):4615-22. doi: 10.1073/pnas.1000082107. Epub 2010 Jul 26.
7
Vitamin D and mucosal immune function.维生素 D 与黏膜免疫功能。
Curr Opin Gastroenterol. 2010 Nov;26(6):591-5. doi: 10.1097/MOG.0b013e32833d4b9f.
8
Viruses in the faecal microbiota of monozygotic twins and their mothers.双歧杆菌在同卵双胞胎及其母亲粪便微生物群中的病毒。
Nature. 2010 Jul 15;466(7304):334-8. doi: 10.1038/nature09199.
9
Immune reconstitution inflammatory syndrome and cerebral toxoplasmosis.免疫重建炎症综合征与脑弓形虫病
AJNR Am J Neuroradiol. 2010 Aug;31(7):E65-6. doi: 10.3174/ajnr.A2158. Epub 2010 May 27.
10
A new vision of immunity: homeostasis of the superorganism.一种新的免疫观:超有机体的内稳态。
Mucosal Immunol. 2010 Sep;3(5):450-60. doi: 10.1038/mi.2010.20. Epub 2010 May 5.

宏基因组时代的免疫刺激。

Immunostimulation in the era of the metagenome.

机构信息

Murdoch University, Perth, WA, Australia.

出版信息

Cell Mol Immunol. 2011 May;8(3):213-25. doi: 10.1038/cmi.2010.77. Epub 2011 Jan 31.

DOI:10.1038/cmi.2010.77
PMID:21278764
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4076734/
Abstract

Microbes are increasingly being implicated in autoimmune disease. This calls for a re-evaluation of how these chronic inflammatory illnesses are routinely treated. The standard of care for autoimmune disease remains the use of medications that slow the immune response, while treatments aimed at eradicating microbes seek the exact opposite-stimulation of the innate immune response. Immunostimulation is complicated by a cascade of sequelae, including exacerbated inflammation, which occurs in response to microbial death. Over the past 8 years, we have collaborated with American and international clinical professionals to research a model-based treatment for inflammatory disease. This intervention, designed to stimulate the innate immune response, has required a reevaluation of disease progression and amelioration. Paramount is the inherent conflict between palliation and microbicidal efficacy. Increased microbicidal activity was experienced as immunopathology-a temporary worsening of symptoms. Further studies are needed, but they will require careful planning to manage this immunopathology.

摘要

微生物越来越多地与自身免疫性疾病有关。这要求我们重新评估这些慢性炎症性疾病的常规治疗方法。自身免疫性疾病的标准治疗方法仍然是使用减缓免疫反应的药物,而旨在消除微生物的治疗方法则寻求完全相反的效果——刺激先天免疫反应。免疫刺激受到一系列后果的影响,包括加剧的炎症,这是对微生物死亡的反应。在过去的 8 年中,我们与美国和国际临床专业人员合作,研究一种基于模型的炎症性疾病治疗方法。这种干预措施旨在刺激先天免疫反应,这需要重新评估疾病的进展和改善。至关重要的是缓解和杀菌效果之间固有的冲突。杀菌活性的增加被认为是免疫病理学——症状的暂时恶化。需要进一步的研究,但需要仔细规划来管理这种免疫病理学。