A recessive form of hyper-IgE syndrome by disruption of ZNF341-dependent STAT3 transcription and activity.

Béziat, Vivien

A recessive form of hyper-IgE syndrome by disruption of ZNF341-dependent STAT3 transcription and activity. [electronic resource] - Science immunology 06 2018

Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

2470-9468

10.1126/sciimmunol.aat4956 doi


Adolescent
Adult
Cell Differentiation--genetics
Cell Nucleus--metabolism
Consanguinity
Cytokines--immunology
Exons--genetics
Female
Gene Expression Regulation--immunology
Genes, Recessive--genetics
Homozygote
Humans
Immunoglobulin E--blood
Job Syndrome--blood
Loss of Function Mutation
Lymphocyte Count
Male
Middle Aged
Pedigree
Promoter Regions, Genetic--genetics
RNA, Messenger--metabolism
STAT3 Transcription Factor--genetics
Th17 Cells--immunology
Th2 Cells--immunology
Transcription Factors--genetics
Transcription, Genetic--immunology
Exome Sequencing
Young Adult
Zinc Fingers--genetics