Cumulative Signaling Through NOD-2 and TLR-4 Eliminates the
NOD-2
TLR-4
autophagy
mesenchymal stem cell
tuberculosis
Journal
Frontiers in cellular and infection microbiology
ISSN: 2235-2988
Titre abrégé: Front Cell Infect Microbiol
Pays: Switzerland
ID NLM: 101585359
Informations de publication
Date de publication:
2021
2021
Historique:
received:
18
02
2021
accepted:
21
06
2021
entrez:
26
7
2021
pubmed:
27
7
2021
medline:
31
7
2021
Statut:
epublish
Résumé
For a long time, tuberculosis (TB) has been inflicting mankind with the highest morbidity and mortality. Although the current treatment is extremely potent, a few bacilli can still hide inside the host mesenchymal stem cells (MSC). The functional capabilities of MSCs are known to be modulated by TLRs, NOD-2, and RIG-1 signaling. Therefore, we hypothesize that modulating the MSC activity through TLR-4 and NOD-2 can be an attractive immunotherapeutic strategy to eliminate the
Identifiants
pubmed: 34307192
doi: 10.3389/fcimb.2021.669168
pmc: PMC8294323
doi:
Substances chimiques
NOD2 protein, human
0
Nod2 Signaling Adaptor Protein
0
TLR4 protein, human
0
Toll-Like Receptor 4
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
669168Informations de copyright
Copyright © 2021 Aqdas, Singh, Amir, Maurya, Pahari and Agrewala.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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