Evidence map›Paper›PMID 27398150›Full record

ArticleAmerican journal of translational research2016

Defects in dermal Vγ4 γ δ T cells result in delayed wound healing in diabetic mice.

Zhongyang Liu, Yingbin Xu, Xiaorong Zhang, Guangping Liang, Lei Chen, Julin Xie, Jinming Tang, Jingling Zhao, Bin Shu, Shaohai Qi and 5 more

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Skin Resident γδ T Cell Function and Regulation in Wound Repair.International journal of molecular sciences · 2020
    Review
  12. Review
  13. CCR6The Journal of investigative dermatology · 2019
    Article
  14. Article
  15. Review
  16. Dermal VγAmerican journal of translational research · 2017
    Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 1 country.

Zhongyang LiuDepartment of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou 510080, Guangdong, China.
Yingbin XuDepartment of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou 510080, Guangdong, China.
Xiaorong ZhangState Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn Research, Southwest Hospital, The Third Military Medical UniversityChongqing 400038, China; Chongqing Key Laboratory for Disease ProteomicsChongqing 400038, China.
Guangping LiangState Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn Research, Southwest Hospital, The Third Military Medical UniversityChongqing 400038, China; Chongqing Key Laboratory for Disease ProteomicsChongqing 400038, China.
Lei ChenDepartment of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou 510080, Guangdong, China.
Julin XieDepartment of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou 510080, Guangdong, China.
Jinming TangDepartment of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou 510080, Guangdong, China.
Jingling ZhaoDepartment of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou 510080, Guangdong, China.
Bin ShuDepartment of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou 510080, Guangdong, China.
Shaohai QiDepartment of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou 510080, Guangdong, China.
Jian ChenState Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn Research, Southwest Hospital, The Third Military Medical UniversityChongqing 400038, China; Chongqing Key Laboratory for Disease ProteomicsChongqing 400038, China.
Gaoxing LuoState Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn Research, Southwest Hospital, The Third Military Medical UniversityChongqing 400038, China; Chongqing Key Laboratory for Disease ProteomicsChongqing 400038, China.
Jun WuState Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn Research, Southwest Hospital, The Third Military Medical UniversityChongqing 400038, China; Chongqing Key Laboratory for Disease ProteomicsChongqing 400038, China.
Weifeng HeState Key Laboratory of Trauma, Burn and Combined Injury, Institute of Burn Research, Southwest Hospital, The Third Military Medical UniversityChongqing 400038, China; Chongqing Key Laboratory for Disease ProteomicsChongqing 400038, China.
Xusheng LiuDepartment of Burns, The First Affiliated Hospital of Sun Yat-sen University Guangzhou 510080, Guangdong, China.
Sun Yat-sen University · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The skin serves as a physical and chemical barrier to provide an initial line of defense against environmental threats; however, this function is impaired in diabetes. Vγ4 γ δ T cells in the dermis are an important part of the resident cutaneous immunosurveillance program, but these cells have yet to be explored in the context of diabetes. In this study, we observed that the impaired maintenance of dermal Vγ4 γ δ T cells is caused by reduced production of IL-7 in the skin of diabetic mice, which was closely associated with weakened activation of the mTOR pathway in the epidermis of diabetic mice. Weakened CCL20/CCR6 chemokine signaling resulted in the impaired recruitment of dermal Vγ4 γ δ T cells following wounding in diabetic mice. Meanwhile, reduced levels of IL-23 and IL-1β in the dermis around the wounds of diabetic mice resulted in the impaired production of IL-17 by dermal Vγ4 γ δ T cells. Therefore, diminished dermal Vγ4 γ δ T cells and impaired IL-17 production by these cells were important factors in the markedly reduced IL-17 levels in the skin around the wounds of diabetic mice. Because reduced IL-17 levels at the wound edge have been closely associated with delayed wound closure in diabetic mice, defects in dermal Vγ4 γ δ T cells may be an important mechanism underlying delayed wound healing in diabetic mice.

Indexed as

dermal Vγ4 γ δ T cellsDiabeteswound healing

Identifiers

PMID27398150
PMCPMC4931161
OpenAlexW2502830972

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.