Cutting Edge: Origins, Recruitment, and Regulation of CD11c(+) Cells in Inflamed Islets of Autoimmune Diabetes Mice.
Cutting Edge: Origins, Recruitment, and Regulation of CD11c(+) Cells in Inflamed Islets of Autoimmune Diabetes Mice.
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DOI：
10.4049/jimmunol.1601062
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发表时间：
2017-07-01
期刊：
影响因子：
--
通讯作者：
Tang Q
中科院分区：
文献类型：
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作者：
Klementowicz JE;Mahne AE;Spence A;Nguyen V;Satpathy AT;Murphy KM;Tang Q
在非肥胖糖尿病小鼠中，CD11c+细胞随着胰岛炎症而大大增加，并有助于胰腺β细胞的自身免疫破坏。在这项研究中，我们调查了他们的起源和招聘机制。炎症胰岛中的CD11c+细胞基于其转录谱类似于经典树突状细胞（DC）。然而，这些细胞中的大多数不是来自Zbtb46依赖性DC谱系。相反，单核细胞前体可以在发炎的胰岛中产生CD11c+细胞。趋化因子CCl 5和CCl 8持续升高，炎症胰岛和流入的CD 11c+细胞部分依赖于其受体Ccr 5。用胰岛抗原特异性调节性T细胞（Tcl4）治疗导致Ccl5和Ccl8的显著减少以及单核细胞募集的减少。这些结果暗示了炎症胰岛中CD11c+细胞的单核细胞起源，并表明治疗性TdR通过改变胰岛中的趋化环境直接或间接调节其流入。
CD11c+ cells increase greatly with islet inflammation in non-obese diabetic mice and contribute to autoimmune destruction of pancreatic beta cells. In this study, we investigated their origin and mechanism of recruitment. CD11c+ cells in inflamed islets resembled classical dendritic cells (DC) based on their transcriptional profile. However, the majority of these cells were not from the Zbtb46-dependent DC lineage. Instead, monocyte precursors could give rise to CD11c+ cells in inflamed islets. Chemokines Ccl5 and Ccl8 were persistently elevated in inflamed islets and the influx of CD11c+ cells was partially dependent on their receptor Ccr5. Treatment with islet antigen-specific regulatory T cells (Tregs) led to a marked decrease of Ccl5 and Ccl8 and a reduction of monocyte recruitment. These results implicate a monocytic origin of CD11c+ cells in inflamed islets and suggest that therapeutic Tregs directly or indirectly regulate their influx by altering the chemotactic milieu in the islets.
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影响因子：
30.5
作者：
通讯作者：
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DOI：
10.4049/jimmunol.0803543
发表时间：
2009-03-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Melli K;Friedman RS;Martin AE;Finger EB;Miao G;Szot GL;Krummel MF;Tang Q
通讯作者：
Tang Q
影响因子：
4.4
作者：
Saxena, Vijay;Ondr, Jennifer K.;Katz, Jonathan D.
通讯作者：
Katz, Jonathan D.
影响因子：
32.4
作者：
Zlotnik A;Yoshie O
通讯作者：
Yoshie O
影响因子：
30.5
作者：
通讯作者：
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