PMID- 33289699
OWN - NLM
STAT- MEDLINE
DCOM- 20210507
LR  - 20210507
IS  - 1945-4589 (Electronic)
IS  - 1945-4589 (Linking)
VI  - 13
IP  - 1
DP  - 2020 Dec 3
TI  - Autophagy-mediated regulation patterns contribute to the alterations of the 
      immune microenvironment in periodontitis.
PG  - 555-577
LID - 10.18632/aging.202165 [doi]
AB  - The relationship between autophagy and immunity has been thoroughly investigated. 
      However, little is known about the role of autophagy in shaping the 
      immune-microenvironment of periodontitis. Thus, we aim to explore the impact of 
      autophagy on the immune-microenvironment of periodontitis. The expression 
      distinctions of autophagy genes between healthy and periodontitis samples have 
      been investigated. The connections between autophagy and immune characteristics 
      including infiltrating immunocyte, immune reaction and human leukocyte antigen 
      (HLA) gene were evaluated. The distinct autophagy-mediated expression patterns 
      were identified and immune characteristics under distinct patterns were revealed. 
      Autophagy phenotype-related genes were identified. 16 autophagy genes were 
      dysregulated and a ten-autophagy classifier was constructed that can well 
      distinguish periodontitis and healthy samples. Immune characteristics were 
      closely related to autophagy: higher expression of EDEM1 positively relates to 
      infiltrating activated B cell; NCKAP1 negatively relates to monocyte; CXCR4 
      enhances BCR Signaling Pathway and PEX3 decreases the activity of TNF Family 
      Members Receptors; positive expression correlation of EDEM1-HLADOB and negative 
      correlation of RAB11A-HLADOB were observed. Two distinct autophagy expression 
      patterns were identified which demonstrated different immune characteristics. 
      4309 autophagy phenotype-related genes were identified, and 219 of them were 
      related to immunity, whose biological functions were found to be involved in 
      immunocyte regulations. Our study revealed the strong impact of autophagy on the 
      immune-microenvironment of periodontitis and brought new insights into the 
      understanding of the pathogenesis of periodontitis.
FAU - Zhang, Xiaoqi
AU  - Zhang X
AD  - Department of Orthodontics, West China Hospital of Stomatology, State Key 
      Laboratory of Oral Diseases, Sichuan University, Chengdu 610041, China.
FAU - Jin, Yu
AU  - Jin Y
AD  - Department of Orthodontics, West China Hospital of Stomatology, State Key 
      Laboratory of Oral Diseases, Sichuan University, Chengdu 610041, China.
FAU - Wang, Qingxuan
AU  - Wang Q
AD  - Department of Orthodontics, West China Hospital of Stomatology, State Key 
      Laboratory of Oral Diseases, Sichuan University, Chengdu 610041, China.
FAU - Jian, Fan
AU  - Jian F
AD  - Department of Orthodontics, West China Hospital of Stomatology, State Key 
      Laboratory of Oral Diseases, Sichuan University, Chengdu 610041, China.
FAU - Li, Minqi
AU  - Li M
AD  - Department of Bone Metabolism, School of Stomatology, Shandong University and 
      Shandong Key Laboratory of Oral Tissue Regeneration and Shandong Engineering 
      Laboratory for Dental Materials and Oral Tissue Regeneration, Jinan 250014, 
      China.
FAU - Long, Hu
AU  - Long H
AD  - Department of Orthodontics, West China Hospital of Stomatology, State Key 
      Laboratory of Oral Diseases, Sichuan University, Chengdu 610041, China.
FAU - Lai, Wenli
AU  - Lai W
AD  - Department of Orthodontics, West China Hospital of Stomatology, State Key 
      Laboratory of Oral Diseases, Sichuan University, Chengdu 610041, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20201203
PL  - United States
TA  - Aging (Albany NY)
JT  - Aging
JID - 101508617
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (CXCR4 protein, human)
RN  - 0 (EDEM1 protein, human)
RN  - 0 (HLA-D Antigens)
RN  - 0 (HLA-DO antigens)
RN  - 0 (Lipoproteins)
RN  - 0 (Membrane Proteins)
RN  - 0 (NCKAP1 protein, human)
RN  - 0 (Peroxins)
RN  - 0 (Pex3 protein, human)
RN  - 0 (Receptors, Antigen, B-Cell)
RN  - 0 (Receptors, CXCR4)
RN  - EC 3.6.1.- (rab11 protein)
RN  - EC 3.6.5.2 (rab GTP-Binding Proteins)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/genetics
MH  - Autophagy/genetics/*immunology
MH  - B-Lymphocytes/immunology
MH  - Case-Control Studies
MH  - Cellular Microenvironment/*immunology
MH  - HLA-D Antigens/genetics
MH  - Humans
MH  - Lipoproteins/genetics
MH  - Membrane Proteins/genetics
MH  - Monocytes/immunology
MH  - Periodontitis/genetics/*immunology
MH  - Peroxins/genetics
MH  - Receptors, Antigen, B-Cell/metabolism
MH  - Receptors, CXCR4/genetics
MH  - Signal Transduction
MH  - Transcriptome
MH  - rab GTP-Binding Proteins/genetics
PMC - PMC7835039
OTO - NOTNLM
OT  - autophagy
OT  - gene expression
OT  - immune microenvironment
OT  - immunity
OT  - periodontitis
COIS- CONFLICTS OF INTEREST: The authors declare no conflicts of interest.
EDAT- 2020/12/09 06:00
MHDA- 2021/05/08 06:00
PMCR- 2021/01/15
CRDT- 2020/12/08 12:31
PHST- 2020/05/21 00:00 [received]
PHST- 2020/10/20 00:00 [accepted]
PHST- 2020/12/09 06:00 [pubmed]
PHST- 2021/05/08 06:00 [medline]
PHST- 2020/12/08 12:31 [entrez]
PHST- 2021/01/15 00:00 [pmc-release]
AID - 202165 [pii]
AID - 10.18632/aging.202165 [doi]
PST - ppublish
SO  - Aging (Albany NY). 2020 Dec 3;13(1):555-577. doi: 10.18632/aging.202165. Epub 
      2020 Dec 3.