Human T-bet governs the generation of a distinct subset of CD11c
Journal
Science immunology
ISSN: 2470-9468
Titre abrégé: Sci Immunol
Pays: United States
ID NLM: 101688624
Informations de publication
Date de publication:
22 07 2022
22 07 2022
Historique:
entrez:
22
7
2022
pubmed:
23
7
2022
medline:
27
7
2022
Statut:
ppublish
Résumé
High-level expression of the transcription factor T-bet characterizes a phenotypically distinct murine B cell population known as "age-associated B cells" (ABCs). T-bet-deficient mice have reduced ABCs and impaired humoral immunity. We describe a patient with inherited T-bet deficiency and largely normal humoral immunity including intact somatic hypermutation, affinity maturation and memory B cell formation in vivo, and B cell differentiation into Ig-producing plasmablasts in vitro. Nevertheless, the patient exhibited skewed class switching to IgG1, IgG4, and IgE, along with reduced IgG2, both in vivo and in vitro. Moreover, T-bet was required for the in vivo and in vitro development of a distinct subset of human B cells characterized by reduced expression of CD21 and the concomitantly high expression of CD19, CD20, CD11c, FCRL5, and T-bet, a phenotype that shares many features with murine ABCs. Mechanistically, human T-bet governed CD21
Identifiants
pubmed: 35867801
doi: 10.1126/sciimmunol.abq3277
pmc: PMC9413977
mid: NIHMS1828447
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
CD11c Antigen
0
Dapp1 protein, mouse
0
Immunoglobulin G
0
Lipoproteins
0
Types de publication
Case Reports
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
eabq3277Subventions
Organisme : Howard Hughes Medical Institute
Pays : United States
Organisme : NIAID NIH HHS
ID : R37 AI095983
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001866
Pays : United States
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