The Role of Innate Lymphoid Cells in the Regulation of Immune Homeostasis in Sepsis-Mediated Lung Inflammation

被引:12
作者
Akama, Yuichi [1 ,2 ]
Satoh-Takayama, Naoko [3 ,4 ]
Kawamoto, Eiji [1 ,2 ]
Ito, Atsushi [1 ,5 ]
Gaowa, Arong [1 ]
Park, Eun Jeong [1 ]
Imai, Hiroshi [2 ]
Shimaoka, Motomu [1 ]
机构
[1] Mie Univ, Grad Sch Med, Dept Mol Pathobiol & Cell Adhes Biol, 2-174 Edobashi, Tsu, Mie 5148507, Japan
[2] Mie Univ, Grad Sch Med, Dept Emergency & Disaster Med, 2-174 Edobashi, Tsu, Mie 5148507, Japan
[3] RIKEN, Lab Intestinal Ecosyst, Ctr Integrat Med Sci, Tsurumi Ku, 1-7-22 Suehiro Cho, Yokohama, Kanagawa 2300045, Japan
[4] Yokohama City Univ, Grad Sch Med Life Sci, Immunobiol Lab, Tsurumi Ku, 1-7-29 Suehiro Cho, Yokohama, Kanagawa 2300045, Japan
[5] Mie Univ, Grad Sch Med, Dept Thorac & Cardiovasc Surg, 2-174 Edobashi, Tsu, Mie 5148507, Japan
关键词
PD-1; group 2 innate lymphoid cells; sepsis; acute lung injury; IL-13; IL-33; ST2; natural and inflammatory ILC2; IL-33; PROMOTES; TYPE-2; IMMUNITY; INJURY; EXPRESSION; PD-1; PROTECTION; PROVIDE; IMMUNOSUPPRESSION; INTERLEUKIN-10; EPIDEMIOLOGY;
D O I
10.3390/diagnostics10100808
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Septic shock/severe sepsis is a deregulated host immune system response to infection that leads to life-threatening organ dysfunction. Lung inflammation as a form of acute lung injury (ALI) is often induced in septic shock. Whereas macrophages and neutrophils have been implicated as the principal immune cells regulating lung inflammation, group two innate lymphoid cells (ILC2s) have recently been identified as a new player regulating immune homeostasis. ILC2 is one of the three major ILC subsets (ILC1s, ILC2s, and ILC3s) comprised of newly identified innate immune cells. These cells are characterized by their ability to rapidly produce type 2 cytokines. ILC2s are predominant resident ILCs and, thereby, have the ability to respond to signals from damaged tissues. ILC2s regulate the immune response, and ILC2-derived type 2 cytokines may exert protective roles against sepsis-induced lung injury. This focused review not only provides readers with new insights into the signaling mechanisms by which ILC2s modulate sepsis-induced lung inflammation, but also proposes ILC2 as a novel therapeutic target for sepsis-induced ALI.
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页数:14
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