Extracellular vesicles produced by primary human keratinocytes in response to TLR agonists induce stimulus-specific responses in antigen-presenting cells.
Autophagy
Cytokine
Extracellular vesicles
Keratinocytes
LC3b-II
Langerhans cells
Toll-like receptor
Journal
Cellular signalling
ISSN: 1873-3913
Titre abrégé: Cell Signal
Pays: England
ID NLM: 8904683
Informations de publication
Date de publication:
07 2021
07 2021
Historique:
received:
23
12
2020
revised:
23
03
2021
accepted:
24
03
2021
pubmed:
31
3
2021
medline:
20
1
2022
entrez:
30
3
2021
Statut:
ppublish
Résumé
Cells can communicate through the extracellular vesicles (EVs) they secrete. Pathogen associated molecular patterns (PAMPs), alter the biophysical and communicative properties of EVs released from cells, but the functional consequences of these changes are unknown. Characterization of keratinocyte-derived EVs after poly(I:C) treatment (poly(I:C)-EVs) showed slight differences in levels of EV markers TSG101 and Alix, a loss of CD63 and were positive for autophagosome marker LC3b-II and the cytokine IL36γ compared to EVs from unstimulated keratinocytes (control-EVs). Flagellin treatment (flagellin-EVs) led to an EV marker profile like control-EVs but lacked LC3b-II. Flagellin-EVs also lacked IL-36γ despite nearly identical intracellular levels. While poly(I:C) treatment led to the clear emergence of a > 200 nm diameter EV sub-population, these were not found in flagellin-EVs. EV associated IL-36γ colocalized with LC3b-II in density gradient analysis, equilibrating to 1.10 g/mL, indicating a common EV species. Poly(I:C), but not flagellin, induced intracellular vesicles positive for IL-36γ, LC3b-II, Alix and TSG101, consistent with fusion of autophagosomes and multivesicular bodies. Simultaneous rapamycin and flagellin treatment induced similar intracellular vesicles but was insufficient for the release of IL-36γ
Identifiants
pubmed: 33781846
pii: S0898-6568(21)00082-6
doi: 10.1016/j.cellsig.2021.109994
pmc: PMC8091864
mid: NIHMS1690702
pii:
doi:
Substances chimiques
HUM 5007
0
Nicotinic Acids
0
Plant Extracts
0
Toll-Like Receptors
0
Cholecalciferol
1C6V77QF41
Dehydroepiandrosterone
459AG36T1B
Poly I-C
O84C90HH2L
Ascorbic Acid
PQ6CK8PD0R
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
109994Subventions
Organisme : NIDCR NIH HHS
ID : R01 DE017227
Pays : United States
Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.
Références
Am J Pathol. 1998 Jun;152(6):1445-52
pubmed: 9626049
Redox Biol. 2019 Feb;21:101080
pubmed: 30584981
Front Immunol. 2020 Mar 10;11:336
pubmed: 32210959
J Invest Dermatol. 2017 Dec;137(12):2620-2629
pubmed: 28774595
Mol Med. 2014 Aug 28;20:372-80
pubmed: 24950037
Sci Rep. 2017 Jul 18;7(1):5676
pubmed: 28720835
Immunology. 2005 Apr;114(4):531-41
pubmed: 15804290
Ann N Y Acad Sci. 2018 Apr;1417(1):23-34
pubmed: 27783881
Cell Death Differ. 2009 Jan;16(1):70-8
pubmed: 19008921
Biochem Biophys Res Commun. 2006 Jan 6;339(1):437-42
pubmed: 16300744
Clin Exp Immunol. 2016 May;184(2):159-73
pubmed: 26701127
Cell Signal. 2007 Apr;19(4):731-9
pubmed: 17112701
Cancers (Basel). 2018 Sep 22;10(10):
pubmed: 30248985
Mol Med. 2018 May 16;24(1):23
pubmed: 30134802
Vet Immunol Immunopathol. 2014 Feb 15;157(3-4):197-205
pubmed: 24461722
Autophagy. 2018;14(1):98-119
pubmed: 29198173
Pharmacol Ther. 2018 May;185:135-146
pubmed: 29274705
J Invest Dermatol. 2015 Aug;135(8):2005-2011
pubmed: 25822580
Virus Res. 2017 Mar 2;231:21-33
pubmed: 27890631
Biochem J. 2009 Sep 14;423(1):119-28
pubmed: 19619129
J Invest Dermatol. 2001 Feb;116(2):313-8
pubmed: 11180009
Blood. 2007 Nov 1;110(9):3234-44
pubmed: 17666571
Cell. 2019 Apr 4;177(2):428-445.e18
pubmed: 30951670
Exp Cell Res. 2017 Dec 1;361(1):46-55
pubmed: 28982539
Toxicol Appl Pharmacol. 2013 Jun 15;269(3):290-6
pubmed: 23566955
Curr Protoc Cell Biol. 2006 Apr;Chapter 3:Unit 3.22
pubmed: 18228490
Respirology. 2016 Apr;21(3):467-75
pubmed: 26804470
J Leukoc Biol. 2020 Jun;107(6):1167-1173
pubmed: 32272490
Autophagy. 2016;12(1):1-222
pubmed: 26799652
Mol Biosyst. 2017 Jun 27;13(7):1291-1296
pubmed: 28488707
Int J Mol Sci. 2018 Nov 27;19(12):
pubmed: 30486423
Nat Rev Mol Cell Biol. 2018 Apr;19(4):213-228
pubmed: 29339798
Aging Dis. 2019 Dec 1;10(6):1302-1310
pubmed: 31788341
J Eur Acad Dermatol Venereol. 2019 Jun;33(6):1177-1188
pubmed: 30720896
Int Arch Allergy Immunol. 1995 May-Jun;107(1-3):233-5
pubmed: 7542074
Immunol Rev. 2018 Jan;281(1):169-178
pubmed: 29247994
Exp Dermatol. 2018 Nov;27(11):1287-1293
pubmed: 30230035
Sci Rep. 2018 Jun 12;8(1):8973
pubmed: 29895824
Discov Med. 2019 May;27(149):201-210
pubmed: 31361983
Open Biol. 2017 Nov;7(11):
pubmed: 29118271
Proc Natl Acad Sci U S A. 2016 Feb 23;113(8):E968-77
pubmed: 26858453
Eur J Immunol. 2015 Sep;45(9):2628-37
pubmed: 26205220
Biomark Med. 2018 Apr;12(4):383-391
pubmed: 29441794
J Cell Physiol. 2019 May;234(5):5683-5699
pubmed: 30341914
Immunol Res. 2015 Dec;63(1-3):228-35
pubmed: 26407986
Nat Cell Biol. 2019 Jan;21(1):9-17
pubmed: 30602770
PLoS Pathog. 2013;9(5):e1003384
pubmed: 23717208
PLoS One. 2010 Jul 26;5(7):e11754
pubmed: 20668677
J Invest Dermatol. 2005 Sep;125(3):499-509
pubmed: 16117791
Int J Mol Sci. 2017 Mar 20;18(3):
pubmed: 28335522
Nat Microbiol. 2019 Feb;4(2):339-351
pubmed: 30510168