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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Vydáno v:	Frontiers in immunology Ročník 14; s. 1067459
Hlavní autoři:	Singh, Amit, Kaileh, Mary, De, Supriyo, Mazan-Mamczarz, Krystyna, Bayarsaihan, Dashzeveg, Sen, Ranjan, Roy, Ananda L.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Switzerland Frontiers Media S.A 23.01.2023
Témata:	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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Shrnutí:	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.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 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