Abstract
The immune system plays a critical role in defense against invading pathogens, and its function must be strictly controlled to maintain intracellular homeostasis. Once suffering microbial invasion or receiving danger signals, the immune system initiates the responses timely. After the threat removal, the immune system should be shut down to avoid the harm caused by excessive immune activation. Additionally, the immune system needs to be internally adjusted so that it does not respond to self-antigens to avoid autoimmune diseases. The states of nonresponse in immunity are termed as immune tolerance. Numerous studies indicated that macroautophagy (hereafter named as autophagy) is involved in T cells and B cells related immune tolerance. Recently, more and more researches demonstrated that autophagy is not only capable of nonselective degradation of cellular macromolecular components but also responsible for sorting and transporting autophagic substrates through a group of cargo receptors for selective degradation, which is called as selective autophagy. Recent studies indicated that selective autophagy can effectively regulate the immune tolerance and avoid over-activation of immune response by targeting multiple receptors and effectors of immune cells. In this chapter, we will focus on how autophagy participates explicitly in the adaptive and innate immune tolerance.
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Abbreviations
- AIM2:
-
Absent in melanoma 2
- AMPK:
-
Adenine monophosphate activated protein kinase
- APC:
-
Antigen-presenting cell
- ASC:
-
Apoptosis-associated speck-like protein containing a CARD
- BMDM:
-
Bone marrow derived macrophages
- caspase:
-
Cysteinyl aspartate specific proteinase
- CCL5:
-
CC chemokine ligand 5
- CD4:
-
Cluster of differentiation 4
- cGAMP:
-
Cyclic guanosine monophosphate–adenosine monophosphate
- cGAS:
-
Cyclic GMP-AMP synthase
- cTEC:
-
Thymic cortical epithelial cell
- CTLA-4:
-
Cytotoxic T-lymphocyte-associated protein 4
- DAMP:
-
Danger-associated molecular pattern
- DC:
-
Dendritic cell
- DP:
-
Double-positive cell
- EGR:
-
Early growth response protein
- FAO:
-
Fatty acid oxidation
- FAS:
-
Fatty acid biosynthesis
- GSDMD:
-
Gasdermin D
- GWAS:
-
Genome-wide association study
- GZMB:
-
Granzyme B
- HFD:
-
High-fat diet
- HSV-1:
-
Herpes simplex virus type 1
- IFN:
-
Interferon
- IKK:
-
IκB kinase
- IL:
-
Interleukin
- ILC:
-
Innate lymphoid cell
- IRF3:
-
Interferon regulatory factor 3
- ISG15:
-
Interferon-stimulated gene 15
- JAK2:
-
Janus kinase 2
- JIA:
-
Juvenile idiopathic arthritis
- LC3:
-
Microtubule-associated proteins light chain 3
- LPS:
-
Lipopolysaccharide
- LRRC25:
-
Leucine-rich repeat-containing protein 25
- MAVS:
-
Mitochondrial antiviral-signaling protein
- MHC:
-
Major histocompatibility complex
- mTOR:
-
Mammalian target of rapamycin
- MyD88:
-
Myeloid differentiation primary response 88
- NBR1:
-
Neighbor of BRCA1 gene 1
- NDP52:
-
Nuclear dot protein 52Â kDa
- NF-κB:
-
Nuclear factor kappa-B
- NK:
-
Natural killer cell
- NLRP3:
-
NACHT, LRR and PYD domains-containing protein 3
- NOD2:
-
Nucleotide-binding oligomerization domain-containing protein 2
- OPTN:
-
Optineurin
- PAI-2:
-
Plasminogen activator inhibitor type 2
- PAMP:
-
Pathogen-associated molecular pattern
- PD1:
-
Programmed cell death protein 1
- PRR:
-
Pattern recognition receptor
- PTPN1:
-
Non receptor type 1
- RIG-I:
-
Retinoic acid-inducible gene I
- ROS:
-
Reactive oxygen species
- SKP2:
-
S-phase kinase-associated protein 2
- STAT1:
-
Signal transducer and activator of transcription 1
- STING:
-
Stimulator of interferon genes protein
- TAK1:
-
Transforming growth factor activated kinase-1
- TBK1:
-
TANK-binding kinase 1
- TCR:
-
T cell receptor
- TGF-β:
-
Transforming growth factor-β
- Th:
-
Helper T cell
- TLR:
-
Toll-like receptor
- TNF:
-
Tumor necrosis factor
- Treg:
-
Regulatory T cell
- TRIF:
-
TIR domain-containing adapter molecule 1
- TRIM:
-
Tripartite motif containing
- ULK1:
-
UNC-51-like kinase 1
- VPS34:
-
Vacuolar protein sorting 34
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Wu, YX., Jin, SH., Cui, J. (2019). Autophagy and Immune Tolerance. In: Qin, ZH. (eds) Autophagy: Biology and Diseases. Advances in Experimental Medicine and Biology, vol 1206. Springer, Singapore. https://doi.org/10.1007/978-981-15-0602-4_28
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DOI: https://doi.org/10.1007/978-981-15-0602-4_28
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