Dectin-1 plays a redundant role in the immunomodulatory activities of β-glucan-rich ligands in vivo

被引:77
作者
Marakalala, Mohlopheni J. [1 ]
Williams, David L. [2 ]
Hoving, Jennifer C. [1 ]
Engstad, Rolf [3 ]
Netea, Mihai G. [4 ]
Brown, Gordon D. [1 ]
机构
[1] Univ Cape Town, Inst Infect Dis & Mol Med, Div Immunol, ZA-7700 Rondebosch, South Africa
[2] E Tennessee State Univ, James H Quillen Coll Med, Dept Surg, Johnson City, TN 37614 USA
[3] Biotec BetaGlucans AS, N-9294 Tromso, Norway
[4] Radboud Univ Nijmegen, Med Ctr, Dept Med, NL-6525 ED Nijmegen, Netherlands
基金
新加坡国家研究基金会; 英国惠康基金; 英国医学研究理事会;
关键词
Innate immunity; Immunomodulation; Dectin-1; Beta-glucan; MODS; Staphylococcus aureus; INCREASED RESISTANCE; IMMUNE-RESPONSES; INFLAMMATION; PARTICULATE; INFECTION; RECEPTOR; DEFENSE; INNATE;
D O I
10.1016/j.micinf.2013.03.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
beta-Glucans are known for their ability to trigger both protective and damaging immune responses. Here we have explored the role of the beta-glucan receptor Dectin-1 in archetypical models of protective and non-protective immunomodulation induced by beta-glucan rich ligands. In the first model, we explored the role of Dectin-1 in the ability of soluble purified beta-glucans to mediate protection against systemic Staphylococcus aureus infection in mice. In the second model, we explored the role of Dectin-1 in zymosan induced multiple organ dysfunction syndrome. In both cases, these beta-glucan rich compounds had marked effects in vivo which were unaltered by Dectin-1 deficiency, suggesting that this receptor has a redundant role in these murine models. (c) 2013 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:511 / 515
页数:5
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