PMID- 37603175
OWN - NLM
STAT- MEDLINE
DCOM- 20230914
LR  - 20230914
IS  - 1940-6029 (Electronic)
IS  - 1064-3745 (Linking)
VI  - 2700
DP  - 2023
TI  - Use of CRISPR/CAS9 Technologies to Study the Role of TLR in Dendritic Cell 
      Subsets.
PG  - 77-92
LID - 10.1007/978-1-0716-3366-3_4 [doi]
AB  - Dendritic cells (DCs) have a significant role in coordinating both innate and 
      adaptive immunity by serving as sentinels that detect invaders and initiate 
      immune responses to eliminate them, as well as presenting antigens to activate 
      adaptive immune responses that are specific to the antigen and the context in 
      which it was detected. The regulation of DC functions is complex and involves 
      intracellular drivers such as transcription factors and signaling pathways, as 
      well as intercellular interactions with adhesion molecules, chemokines, and their 
      receptors in the microenvironment. Toll-like receptors (TLRs) are crucial for DCs 
      to detect pathogen-associated molecular patterns (PAMPs) and initiate downstream 
      signaling pathways that lead to DC maturation and education in bridging with 
      adaptive immunity, including the upregulation of MHC class II expression, 
      induction of CD80, CD86, and CD40, and production of innate cytokines. 
      Understanding the TLR pathways that DCs use to respond to innate immune stimuli 
      and convert them into adaptive responses is important for new therapeutic targets 
      identification.We present a novel platform that offers a fast and affordable 
      CRISPR-Cas9 screening of genes that are involved in dendritic cells' 
      TLR-dependent activation. Using CRISPR/Cas9 screening to target individual TLR 
      genes in different dendritic cell subsets allows the identification of 
      TLR-dependent pathways that regulate dendritic cell activation and cytokine 
      production. This approach offers the efficient targeting of TLR driver genes to 
      modulate the immune response and identify novel immune response regulators, 
      establishing a causal link between these regulators and functional phenotypes 
      based on genotypes.
CI  - (c) 2023. The Author(s), under exclusive license to Springer Science+Business 
      Media, LLC, part of Springer Nature.
FAU - Mencarelli, Giulia
AU  - Mencarelli G
AD  - Department of Medicine and Surgery, University of Perugia, Perugia, Italy.
FAU - Pieroni, Benedetta
AU  - Pieroni B
AD  - Department of Medicine and Surgery, University of Perugia, Perugia, Italy.
FAU - Murphy, Kenneth M
AU  - Murphy KM
AD  - Department of Pathology and Immunology, Washington University in St. Louis, 
      School of Medicine, St. Louis, MO, USA.
FAU - Gargaro, Marco
AU  - Gargaro M
AD  - Department of Medicine and Surgery, University of Perugia, Perugia, Italy. 
      marco.gargaro@unipg.it.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Methods Mol Biol
JT  - Methods in molecular biology (Clifton, N.J.)
JID - 9214969
RN  - 0 (Toll-Like Receptors)
RN  - 0 (Cytokines)
SB  - IM
MH  - CRISPR-Cas Systems
MH  - Toll-Like Receptors/genetics/metabolism
MH  - *Dendritic Cells/metabolism
MH  - Animals
MH  - Mice
MH  - Cytokines/metabolism
MH  - Intracellular Space/metabolism
OTO - NOTNLM
OT  - CRISPR/CAS9
OT  - Cytokines
OT  - Dendritic cell subsets
OT  - Retroviral vectors
OT  - Toll-like receptors
EDAT- 2023/08/21 12:42
MHDA- 2023/08/22 06:42
CRDT- 2023/08/21 11:09
PHST- 2023/08/22 06:42 [medline]
PHST- 2023/08/21 12:42 [pubmed]
PHST- 2023/08/21 11:09 [entrez]
AID - 10.1007/978-1-0716-3366-3_4 [doi]
PST - ppublish
SO  - Methods Mol Biol. 2023;2700:77-92. doi: 10.1007/978-1-0716-3366-3_4.