Invariant NKT cells promote skin wound healing by preventing a prolonged neutrophilic inflammatory response

被引：40

作者：

Tanno, Hiromasa ^{[1
]}

Kawakami, Kazuyoshi ^{[2
]}

Kanno, Emi ^{[1
]}

Suzuki, Aiko ^{[3
]}

Takagi, Naoyuki ^{[3
]}

Yamamoto, Hideki ^{[2
,4
]}

Ishii, Keiko ^{[2
]}

Imai, Yoshimichi ^{[3
]}

Maruyama, Ryoko ^{[1
]}

Tachi, Masahiro ^{[3
]}

机构：

[1] Tohoku Univ, Grad Sch Med, Dept Sci Nursing Practice, Sendai, Miyagi, Japan

[2] Tohoku Univ, Grad Sch Med, Dept Med Microbiol Mycol & Immunol, Sendai, Miyagi, Japan

[3] Tohoku Univ, Grad Sch Med, Dept Plast & Reconstruct Surg, Sendai, Miyagi, Japan

[4] Niigata Univ, Ctr Transdisciplinary Res, Nishi Ku, 8050 Ikarashi,2 No Cho, Niigata, Japan

来源：

WOUND REPAIR AND REGENERATION | 2017年 / 25卷 / 05期

关键词：

KILLER T-CELLS; IFN-GAMMA; EXPRESSION; REPAIR; REQUIREMENT; LEUKOCYTE; CHEMOKINE; ELASTASE; IL-17;

D O I：

10.1111/wrr.12588

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The wound-healing process consists of the inflammation, proliferation, and remodeling phases. In chronic wounds, the inflammation phase is prolonged with persistent neutrophil infiltration. The inflammatory response is critically regulated by cytokines and chemokines that are secreted from various immune cells. Recently, we showed that skin wound healing was delayed and the healing process was impaired under conditions lacking invariant natural killer T (iNKT) cells, an innate immune lymphocyte with potent immuno-regulatory activity. In the present study, we investigated the effect of iNKT cell deficiency on the neutrophilic inflammatory response during the wound healing process. Neutrophil infiltration was prolonged in wound tissue in mice genetically lacking iNKT cells (J18KO mice) than in wild-type (WT) control mice on days 1 and 3 after wounding. MIP-2, KC, and IL-17A were produced at a significantly higher level in J18KO mice than in WT mice. In addition, neutrophil apoptosis was significantly reduced in the wound tissue in J18KO mice than in WT mice. Treatment with anti-IL-17A mAb, anti-Gr-1 mAb, or neutrophil elastase inhibitor reversed the impaired wound healing in J18KO mice. These results suggest that iNKT cells may promote the wound healing process through preventing the prolonged inflammatory response mediated by neutrophils.

引用

页码：805 / 815

页数：11