Transcription factor TFII-I fine tunes innate properties of B lymphocytes

The ubiquitously expressed transcription factor TFII-I is a multifunctional protein with pleiotropic roles in gene regulation. TFII-I associated polymorphisms are implicated in Sjögren’s syndrome and Lupus in humans and, germline deletion of the Gtf2i gene in mice leads to embryonic lethality. Here...

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Veröffentlicht in:Frontiers in immunology Jg. 14; S. 1067459
Hauptverfasser: Singh, Amit, Kaileh, Mary, De, Supriyo, Mazan-Mamczarz, Krystyna, Bayarsaihan, Dashzeveg, Sen, Ranjan, Roy, Ananda L.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Switzerland Frontiers Media S.A 23.01.2023
Schlagworte:
Animals
B cell
Chromatin
chromatin accessibility
FO and MZ B cells
Gtf2i
Humans
Immunology
innate and adaptive immunity
Mice
Protein Binding
Sjogren's Syndrome
Transcription Factors - genetics
Transcription Factors - metabolism
Transcription Factors, TFII - genetics
Transcription Factors, TFII - metabolism
Transcription Factors, TFIII - genetics
Transcription Factors, TFIII - metabolism
B cell
FO and MZ B cells
innate and adaptive immunity
Gtf2i
chromatin accessibility
ISSN:1664-3224, 1664-3224
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Zusammenfassung:The ubiquitously expressed transcription factor TFII-I is a multifunctional protein with pleiotropic roles in gene regulation. TFII-I associated polymorphisms are implicated in Sjögren’s syndrome and Lupus in humans and, germline deletion of the Gtf2i gene in mice leads to embryonic lethality. Here we report a unique role for TFII-I in homeostasis of innate properties of B lymphocytes. Loss of Gtf2i in murine B lineage cells leads to an alteration in transcriptome, chromatin landscape and associated transcription factor binding sites, which exhibits myeloid-like features and coincides with enhanced sensitivity to LPS induced gene expression. TFII-I deficient B cells also show increased switching to IgG3, a phenotype associated with inflammation. These results demonstrate a role for TFII-I in maintaining immune homeostasis and provide clues for GTF2I polymorphisms associated with B cell dominated autoimmune diseases in humans.
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SourceType-Scholarly Journals-1
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content type line 23
Edited by: Hermann Eibel, University of Freiburg Medical Center, Germany
Reviewed by: Reuben Matthew Tooze, University of Leeds, United Kingdom; Stephen Nutt, The University of Melbourne, Australia
These authors share first authorship
This article was submitted to B Cell Biology, a section of the journal Frontiers in Immunology
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2023.1067459