NFATc1 induction by an intronic enhancer restricts NKT γδ cell formation.
Immunology
developmental biology
molecular biology
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
17 Mar 2023
17 Mar 2023
Historique:
received:
19
04
2022
revised:
08
06
2022
accepted:
13
02
2023
entrez:
17
3
2023
pubmed:
18
3
2023
medline:
18
3
2023
Statut:
epublish
Résumé
In thymus, the ablation of T cell receptor (TCR)-activated transcription factor NFATc1 or its inducible isoforms during the double-negative (DN) stages of thymocyte development leads to a marked increase in γδ thymocytes whereas the development of αβ thymocytes remains mostly unaffected. These γδ thymocytes are characterized by the upregulation of the promyelocytic leukemia zinc-finger factor (PLZF), the "master regulator" of natural killer T (NKT) cell development, and the acquisition of an NKT γδ cell phenotype with higher cell survival rates. The suppressive function of NFATc1 in NKT γδ cell formation critically depends on the remote enhancer E2, which is essential for the inducible expression of NFATc1 directed by its distal promoter P1. Thus, the enhancer deciphers a strong γδ TCR signal into the expression of inducible NFATc1 isoforms resulting in high levels of NFATc1 protein that are essential to control the numbers of NKT γδ cells.
Identifiants
pubmed: 36926655
doi: 10.1016/j.isci.2023.106234
pii: S2589-0042(23)00311-5
pmc: PMC10011748
doi:
Types de publication
Journal Article
Langues
eng
Pagination
106234Informations de copyright
© 2023 The Author(s).
Déclaration de conflit d'intérêts
The authors declare no competing interests.
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