PMID- 38305335
OWN - NLM
STAT- MEDLINE
DCOM- 20240205
LR  - 20240307
IS  - 1040-8401 (Print)
IS  - 1040-8401 (Linking)
VI  - 44
IP  - 2
DP  - 2024
TI  - MicroRNA-99b Regulates Bacillus Calmette-Guerin-Infected Immature Dendritic 
      Cell-Induced CD4+ T Cell Differentiation by Targeting mTOR Signaling.
PG  - 35-47
LID - 10.1615/CritRevImmunol.2023050312 [doi]
AB  - This study aimed to elucidate the mechanisms by which microRNA-99b (miR-99b) 
      regulates CD4+ T cell differentiation induced by Bacillus Calmette-Guerin 
      (BCG)-infected immature dendritic cells (imDCs). Levels of miR-99b, 
      interferon-gamma (IFN-gamma), Foxp3, interleukin (IL)-10, IL-17, IL-23, and ROR-gammat 
      were assessed. Effects of miR-99b inhibition and mechanistic target of rapamycin 
      (mTOR) agonist on Th17/Treg cell ratio and cytokine levels (IL-6, IL-17, IL-23) 
      were studied. Expression of mTOR, S6K1, and 4E-BP1 related to miR-99b was 
      analyzed. BCG-infected imDCs led to CD4+ T cell differentiation and altered 
      levels of IFN-gamma, Foxp3, IL-10, miR-99b, IL-17, IL-23, and ROR-gammat. Inhibition of 
      miR-99b increased the Th17/Treg cell ratio in CD4+ T cells co-cultured with 
      BCG-infected imDCs, and this effect was further enhanced by the mTOR agonist. 
      Additionally, the miR-99b inhibitor elevated the levels of IL-6, IL-17, and IL-23 
      when CD4+ T cells were co-cultured with BCG-infected imDCs, and the mTOR agonist 
      further amplified this increase. Notably, miR-99b negatively regulated mTOR 
      signaling, as the miR-99b inhibitor upregulated the expression levels of mTOR, 
      S6K1, and 4E-BP1 while decreasing miR-99b. It was concluded that miR-99b 
      modulates CD4+ T cell differentiation via mTOR pathway in response to 
      BCG-infected im-DCs. Inhibiting miR-99b affects Th17/Treg ratio and 
      pro-inflammatory cytokines, potentially impacting tuberculosis immunotherapies.
FAU - Zhen, Libo
AU  - Zhen L
AD  - Department of Tuberculosis, Affiliated Hangzhou Chest Hospital, Zhejiang 
      University School of Medicine, Hangzhou 310030, China.
FAU - Chen, Yuanyuan
AU  - Chen Y
AD  - Tuberculosis Laboratory, Affiliated Hangzhou Chest Hospital, Zhejiang University 
      School of Medicine, Hangzhou 310030, China.
FAU - Gao, Juwei
AU  - Gao J
AD  - Department of Oncology, The Third Affiliated Hospital of Zhejiang Chinese Medical 
      University, Hangzhou 310061, China.
FAU - Li, Boying
AU  - Li B
AD  - Department of Tuberculosis, Affiliated Hangzhou Chest Hospital, Zhejiang 
      University School of Medicine, Hangzhou 310030, China.
FAU - Jia, Yangmin
AU  - Jia Y
AD  - Department of Occupational Medicine, Affiliated Hangzhou Chest Hospital, Zhejiang 
      University School of Medicine, Hangzhou 310030, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Crit Rev Immunol
JT  - Critical reviews in immunology
JID - 8914819
RN  - 0 (BCG Vaccine)
RN  - 0 (Cytokines)
RN  - 0 (Forkhead Transcription Factors)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 0 (Interleukin-17)
RN  - 0 (Interleukin-23)
RN  - 0 (Interleukin-6)
RN  - 0 (MicroRNAs)
RN  - 0 (Nuclear Receptor Subfamily 1, Group F, Member 3)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Humans
MH  - BCG Vaccine
MH  - CD4-Positive T-Lymphocytes
MH  - Cell Differentiation
MH  - Cytokines/metabolism
MH  - Dendritic Cells
MH  - Forkhead Transcription Factors
MH  - Interferon-gamma
MH  - Interleukin-17
MH  - Interleukin-23
MH  - Interleukin-6
MH  - *MicroRNAs/genetics
MH  - *Mycobacterium bovis/metabolism
MH  - Nuclear Receptor Subfamily 1, Group F, Member 3/genetics
MH  - TOR Serine-Threonine Kinases/metabolism
EDAT- 2024/02/02 12:42
MHDA- 2024/02/05 06:43
CRDT- 2024/02/02 09:27
PHST- 2024/02/05 06:43 [medline]
PHST- 2024/02/02 12:42 [pubmed]
PHST- 2024/02/02 09:27 [entrez]
AID - 282f3b6c1c729c6a,14bdc2ad74746b8b [pii]
AID - 10.1615/CritRevImmunol.2023050312 [doi]
PST - ppublish
SO  - Crit Rev Immunol. 2024;44(2):35-47. doi: 10.1615/CritRevImmunol.2023050312.