δείτε την πρωτότυπη σελίδα τεκμηρίου στον ιστότοπο του αποθετηρίου του φορέα για περισσότερες πληροφορίες και για να δείτε όλα τα ψηφιακά αρχεία του τεκμηρίου*
Διερευνώντας τον ρόλο του cMaf ως ρυθμιστή της αυτοανοσίας
Investigating cMaf as a key driver of autoimmunity
Special AT-rich Sequence-Binding Protein 1 (SATB1) is a lineage specific transcription regulator
which plays a pivotal role in orchestrating the spatiotemporal development of T cells. Although it
is known that SATB1 deletion is associated with autoimmunity, the precise mechanisms
underlying this phenotype are poorly understood. In this study we investigate the drivers of the
autoimmunity that SATB1 deletion causes and how it is reversed upon simultaneous deletion of
SATB1 and Bach1. We performed single cell transcriptomic analysis, and identified a newly
formed cluster, characterized by the expression of cMaf. Furthermore, using an array of
bioinformatic tools we discovered that this unique cluster exhibits an activated phenotype,
seemingly regulated by cMaf. Additionally, immunofluorescence experiments unveiled disrupted
spleen morphology in SATB1-depleted animals, a disruption absent in animals with combined
SATB1 and Bach1 depletion. Altogether, our findings highlight cMaf a mediator of autoimmunity,
and strengthen the notion that double SATB1 and BACH1 depletion rescues the autoimmune
phenotype.
(EL)
Special AT-rich Sequence-Binding Protein 1 (SATB1) is a lineage specific transcription regulator
which plays a pivotal role in orchestrating the spatiotemporal development of T cells. Although it
is known that SATB1 deletion is associated with autoimmunity, the precise mechanisms
underlying this phenotype are poorly understood. In this study we investigate the drivers of the
autoimmunity that SATB1 deletion causes and how it is reversed upon simultaneous deletion of
SATB1 and Bach1. We performed single cell transcriptomic analysis, and identified a newly
formed cluster, characterized by the expression of cMaf. Furthermore, using an array of
bioinformatic tools we discovered that this unique cluster exhibits an activated phenotype,
seemingly regulated by cMaf. Additionally, immunofluorescence experiments unveiled disrupted
spleen morphology in SATB1-depleted animals, a disruption absent in animals with combined
SATB1 and Bach1 depletion. Altogether, our findings highlight cMaf a mediator of autoimmunity,
and strengthen the notion that double SATB1 and BACH1 depletion rescues the autoimmune
phenotype.
(EN)
*Η εύρυθμη και αδιάλειπτη λειτουργία των διαδικτυακών διευθύνσεων των συλλογών (ψηφιακό αρχείο, καρτέλα τεκμηρίου στο αποθετήριο) είναι αποκλειστική ευθύνη των αντίστοιχων Φορέων περιεχομένου.
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