Immunosuppressive MDSCs induced by TLR signaling during infection and role in resolution of inflammation.
Immunosuppressive MDSCs induced by TLR signaling during infection and role in resolution of inflammation.
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DOI：
10.3389/fcimb.2013.00052
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发表时间：
2013
影响因子：
5.7
通讯作者：
Ray P
中科院分区：
文献类型：
--
作者：
Ray A;Chakraborty K;Ray P
配体介导的Toll样受体(Toll-like Receptor，TLRs)的激活不仅可以诱导炎症，还可以抑制免疫，这是一个新兴的研究领域。已经描述了多种负反馈细胞内机制，这些机制发挥作用以防止不受控制的TLR激活。然而，TLR诱导的调节性髓系细胞的鉴定是一个相对较新的发展，在病原体诱导的疾病状态以及癌症中都有影响。我们努力了解高剂量的脂多糖(LPS4)是如何抑制过敏性呼吸道炎症的，从而导致鉴定出CD11b+Griint(Ly6Gint)F4/80+的髓系细胞，它们在表型和形态上与髓系抑制细胞(MDSCs)相似，后者是在癌症背景下最好的研究对象。MDSCs在感染各种细菌、寄生虫和病毒期间也被检测到，这些细菌、寄生虫和病毒可以接触不同的TLR。这些TLR诱导的髓系细胞产生不同类型的介质来影响免疫反应和炎症，这可能对宿主有利，也可能对宿主不利。TLR4/MyD88触发的肺内MDSCs的一个有益功能是吞噬凋亡的中性粒细胞，帮助化解细菌性肺炎期间引发的炎症。更好地了解这些调节细胞的产生和功能将有助于利用它们的潜力或抑制它们的疾病特异性免疫调节功能。
Ligand-mediated activation of toll-like receptors (TLRs) not only induces inflammation but also immune suppression, which is an emerging area of investigation. Multiple negative feedback intracellular mechanisms have been described that are brought into play to prevent uncontrolled TLR activation. However, the identification of TLR-induced regulatory myeloid cells is a relatively recent development that has ramifications in pathogen-induced disease state as well as in cancer. Our efforts to understand how a high dose of lipopolysaccharide (LPS), a ligand of TLR4, suppresses allergic airway inflammation led to the identification of myeloid cells that are CD11b+Griint(Ly6Gint)F4/80+ and are phenotypically and morphologically similar to myeloid-derived suppressor cells (MDSCs) which are best studied in the context of cancer. MDSCs have been also detected during infection by various bacteria, parasites and viruses, which can engage different TLRs. These TLR-induced myeloid cells produce different types of mediators to influence immune response and inflammation that can be either beneficial or detrimental to the host. One beneficial function of TLR4/MyD88-triggered MDSCs in the lung is to efferocytose apoptotic neutrophils to help resolve inflammation elicited during bacterial pneumonia. A better understanding of the generation and function of these regulatory cells would be helpful to harness their potential or suppress their function for disease-specific immune regulation.
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影响因子：
3.1
作者：
BrougHolub, E;Toews, GB;Standiford, TJ
通讯作者：
Standiford, TJ
影响因子：
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Bunt, Stephanie K.;Clements, Virginia K.;Ostrand-Rosenberg, Suzanne
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Ostrand-Rosenberg, Suzanne
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4.9
作者：
Bergeron, Y;Deslauriers, AM;Bergeron, MG
通讯作者：
Bergeron, MG
影响因子：
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作者：
Abraham, E
通讯作者：
Abraham, E
TLR4/MyD88 诱导的 CD11b+Gr-1 int F4/80+ 非迁移性骨髓细胞抑制肺部的 Th2 效应器功能。
影响因子：
8
作者：
Arora, M.;Poe, S. L.;Oriss, T. B.;Krishnamoorthy, N.;Yarlagadda, M.;Wenzel, S. E.;Billiar, T. R.;Ray, A.;Ray, P.
通讯作者：
Ray, P.