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本文引用的文献

1
Long-term control of Mycobacterium bovis BCG infection in the absence of Toll-like receptors (TLRs): investigation of TLR2-, TLR6-, or TLR2-TLR4-deficient mice.在缺乏Toll样受体（TLR）的情况下对卡介苗（Mycobacterium bovis BCG）感染的长期控制：对TLR2、TLR6或TLR2-TLR4缺陷小鼠的研究。
Infect Immun. 2004 Dec;72(12):6994-7004. doi: 10.1128/IAI.72.12.6994-7004.2004.
2
Chronic pneumonia despite adaptive immune response to Mycobacterium bovis BCG in MyD88-deficient mice.在MyD88缺陷小鼠中，尽管对卡介苗（Mycobacterium bovis BCG）有适应性免疫反应，但仍发生慢性肺炎。
Lab Invest. 2004 Oct;84(10):1305-21. doi: 10.1038/labinvest.3700149.
3
MyD88-deficient mice display a profound loss in resistance to Mycobacterium tuberculosis associated with partially impaired Th1 cytokine and nitric oxide synthase 2 expression.MyD88基因缺陷型小鼠对结核分枝杆菌的抵抗力严重丧失，这与Th1细胞因子和一氧化氮合酶2表达部分受损有关。
Infect Immun. 2004 Apr;72(4):2400-4. doi: 10.1128/IAI.72.4.2400-2404.2004.
4
Toll-like receptor 2 (TLR2)-dependent-positive and TLR2-independent-negative regulation of proinflammatory cytokines by mycobacterial lipomannans.分枝杆菌脂甘露聚糖对促炎细胞因子的Toll样受体2（TLR2）依赖性正向调节和TLR2非依赖性负向调节
J Immunol. 2004 Apr 1;172(7):4425-34. doi: 10.4049/jimmunol.172.7.4425.
5
Toll-like receptor 2-deficient mice succumb to Mycobacterium tuberculosis infection.Toll样受体2缺陷型小鼠易死于结核分枝杆菌感染。
Am J Pathol. 2004 Jan;164(1):49-57. doi: 10.1016/S0002-9440(10)63095-7.
6
Mycobacterial infection in MyD88-deficient mice.MyD88基因缺陷小鼠中的分枝杆菌感染
Microbiol Immunol. 2003;47(11):841-7. doi: 10.1111/j.1348-0421.2003.tb03450.x.
7
Mice lacking myeloid differentiation factor 88 display profound defects in host resistance and immune responses to Mycobacterium avium infection not exhibited by Toll-like receptor 2 (TLR2)- and TLR4-deficient animals.缺乏髓样分化因子88的小鼠在宿主抗性以及对鸟分枝杆菌感染的免疫反应方面表现出严重缺陷，而Toll样受体2（TLR2）和Toll样受体4（TLR4）缺陷的动物则未表现出这些缺陷。
J Immunol. 2003 Nov 1;171(9):4758-64. doi: 10.4049/jimmunol.171.9.4758.
8
Control of Mycobacterium bovis BCG infection with increased inflammation in TLR4-deficient mice.卡介苗感染牛分枝杆菌在Toll样受体4缺陷小鼠中炎症增强的控制
Microbes Infect. 2003 Oct;5(12):1070-81. doi: 10.1016/j.micinf.2003.06.001.
9
MyD88 primes macrophages for full-scale activation by interferon-gamma yet mediates few responses to Mycobacterium tuberculosis.髓样分化因子88（MyD88）使巨噬细胞做好被γ干扰素全面激活的准备，但介导的对结核分枝杆菌的反应却很少。
J Exp Med. 2003 Oct 6;198(7):987-97. doi: 10.1084/jem.20030603. Epub 2003 Sep 29.
10
Reactivation of latent tuberculosis infection in TNF-deficient mice.肿瘤坏死因子缺陷小鼠中潜伏性结核感染的再激活。
J Immunol. 2003 Sep 15;171(6):3110-8. doi: 10.4049/jimmunol.171.6.3110.

尽管在缺乏髓样分化因子88（MyD88）的情况下存在适应性免疫反应，但仍发生致命的结核分枝杆菌感染。

Fatal Mycobacterium tuberculosis infection despite adaptive immune response in the absence of MyD88.

作者信息

Fremond Cecile M, Yeremeev Vladimir, Nicolle Delphine M, Jacobs Muazzam, Quesniaux Valerie F, Ryffel Bernhard

机构信息

CNRS, Molecular Immunology and Embryology, 3B rue de la Férollerie, 45071 Orléans, France.

出版信息

J Clin Invest. 2004 Dec;114(12):1790-9. doi: 10.1172/JCI21027.

DOI:10.1172/JCI21027
PMID:15599404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC535064/
Abstract

Toll-like receptors (TLRs) such as TLR2 and TLR4 have been implicated in host response to mycobacterial infection. Here, mice deficient in the TLR adaptor molecule myeloid differentiation factor 88 (MyD88) were infected with Mycobacterium tuberculosis (MTB). While primary MyD88(-/-) macrophages and DCs are defective in TNF, IL-12, and NO production in response to mycobacterial stimulation, the upregulation of costimulatory molecules CD40 and CD86 is unaffected. Aerogenic infection of MyD88(-/-) mice with MTB is lethal within 4 weeks with 2 log(10) higher CFU in the lung; high pulmonary levels of cytokines and chemokines; and acute, necrotic pneumonia, despite a normal T cell response with IFN-gamma production to mycobacterial antigens upon ex vivo restimulation. Vaccination with Mycobacterium bovis bacillus Calmette-Guerin conferred a substantial protection in MyD88(-/-) mice from acute MTB infection. These data demonstrate that MyD88 signaling is dispensable to raise an acquired immune response to MTB. Nonetheless, this acquired immune response is not sufficient to compensate for the profound innate immune defect and the inability of MyD88(-/-) mice to control MTB infection.

摘要

Toll样受体（TLRs），如TLR2和TLR4，已被证明参与宿主对分枝杆菌感染的反应。在此，用结核分枝杆菌（MTB）感染缺乏TLR衔接分子髓样分化因子88（MyD88）的小鼠。虽然原代MyD88（-/-）巨噬细胞和树突状细胞（DCs）在对分枝杆菌刺激的反应中，肿瘤坏死因子（TNF）、白细胞介素-12（IL-12）和一氧化氮（NO）的产生存在缺陷，但共刺激分子CD40和CD86的上调不受影响。用MTB对MyD88（-/-）小鼠进行气溶胶感染在4周内是致命的，肺部的菌落形成单位（CFU）高出2个对数（10）；肺部细胞因子和趋化因子水平较高；以及急性坏死性肺炎，尽管在体外再刺激时对分枝杆菌抗原产生干扰素-γ（IFN-γ）的T细胞反应正常。用卡介苗（Mycobacterium bovis bacillus Calmette-Guerin）接种可使MyD88（-/-）小鼠免受急性MTB感染。这些数据表明MyD88信号传导对于引发针对MTB的获得性免疫反应并非必需。尽管如此，这种获得性免疫反应不足以弥补MyD88（-/-）小鼠严重的先天性免疫缺陷以及控制MTB感染的能力不足。