PMID- 34734243
OWN - NLM
STAT- MEDLINE
DCOM- 20220506
LR  - 20220506
IS  - 1460-2377 (Electronic)
IS  - 0953-8178 (Linking)
VI  - 34
IP  - 3
DP  - 2022 Feb 23
TI  - Transcription factor MafB-mediated inhibition of type I interferons in 
      plasmacytoid dendritic cells.
PG  - 159-172
LID - 10.1093/intimm/dxab103 [doi]
AB  - Type I IFNs (IFN-alpha and IFN-beta), immunomodulatory cytokines secreted from activated 
      plasmacytoid dendritic cells (pDCs), contribute to the innate defense against 
      pathogenic infections and the pathogenesis of the autoimmune disease psoriasis 
      vulgaris. A previous study has shown that an E26 transformation-specific (Ets) 
      family transcription factor Spi-B can transactivate the type I IFN promoter in 
      synergy with IFN regulatory factor (IRF)-7 and is required for type I IFN 
      production in pDCs. However, the mechanism of negative regulation of type I IFNs 
      by pDCs remains unknown. In this study, we report that a basic leucine zipper 
      (bZip) transcription factor v-maf musculoaponeurotic fibrosarcoma oncogene 
      homolog B (MafB) suppresses the induction of type I IFNs in pDCs. The elevated 
      expression of MafB inhibited the transactivation of type I IFN genes in a 
      dose-dependent manner. At the molecular level, MafB interacted with the Ets 
      domain of Spi-B and interfered with IRF-7-Spi-B complexation. Decreased MafB mRNA 
      expression and degradation of MafB protein in the early phase of immune responses 
      led to the enhancement of type I IFNs in pDCs. In vivo studies indicated that 
      MafB is involved in resistance against imiquimod-induced psoriasis-like skin 
      inflammation. Overall, these findings demonstrate that MafB acts as a negative 
      regulator of type I IFN induction in pDCs and plays an important role in 
      maintaining immune homeostasis.
CI  - (c) The Japanese Society for Immunology. 2021. All rights reserved. For 
      permissions, please e-mail: journals.permissions@oup.com.
FAU - Saiga, Hiroyuki
AU  - Saiga H
AUID- ORCID: 0000-0001-9189-4043
AD  - Department of Immunology, Faculty of Medicine, Kagawa University, Miki, Kagawa, 
      Japan.
FAU - Ueno, Masaki
AU  - Ueno M
AD  - Department of Pathology and Host Defense, Faculty of Medicine, Kagawa University, 
      Miki, Kagawa, Japan.
FAU - Tanaka, Takashi
AU  - Tanaka T
AD  - Laboratory for Inflammatory Regulation, RIKEN Center for Integrative Medical 
      Science (IMS-RCAI), Yokohama, Kanagawa, Japan.
FAU - Kaisho, Tsuneyasu
AU  - Kaisho T
AD  - Laboratory for Inflammatory Regulation, RIKEN Center for Integrative Medical 
      Science (IMS-RCAI), Yokohama, Kanagawa, Japan.
AD  - Department of Immunology, Institute of Advanced Medicine, Wakayama Medical 
      University, Kimiidera, Wakayama, Japan.
FAU - Hoshino, Katsuaki
AU  - Hoshino K
AUID- ORCID: 0000-0003-0493-4815
AD  - Department of Immunology, Faculty of Medicine, Kagawa University, Miki, Kagawa, 
      Japan.
AD  - Laboratory for Inflammatory Regulation, RIKEN Center for Integrative Medical 
      Science (IMS-RCAI), Yokohama, Kanagawa, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Int Immunol
JT  - International immunology
JID - 8916182
RN  - 0 (Interferon Type I)
RN  - 0 (Interferon-alpha)
RN  - 0 (MAFB protein, human)
RN  - 0 (MafB Transcription Factor)
SB  - IM
MH  - Dendritic Cells
MH  - Humans
MH  - *Interferon Type I/metabolism
MH  - Interferon-alpha/metabolism
MH  - MafB Transcription Factor/genetics/metabolism
MH  - Promoter Regions, Genetic
MH  - *Psoriasis
OTO - NOTNLM
OT  - autoimmune disease
OT  - innate immunity
OT  - psoriasis
EDAT- 2021/11/05 06:00
MHDA- 2022/05/07 06:00
CRDT- 2021/11/04 06:34
PHST- 2021/04/01 00:00 [received]
PHST- 2021/11/01 00:00 [accepted]
PHST- 2021/11/05 06:00 [pubmed]
PHST- 2022/05/07 06:00 [medline]
PHST- 2021/11/04 06:34 [entrez]
AID - 6420429 [pii]
AID - 10.1093/intimm/dxab103 [doi]
PST - ppublish
SO  - Int Immunol. 2022 Feb 23;34(3):159-172. doi: 10.1093/intimm/dxab103.