JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, vol.124, no.2, pp.342-348, 2009 (Journal Indexed in SCI)
Article / Article
Title of Journal :
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Hyper IgE syndrome, STAT3, T(H)17, IL-6, IL-21, ROR gamma t, UNPHOSPHORYLATED STAT3, CELL-DIFFERENTIATION, MUTATIONS, ROLES, PHOSPHORYLATION, DEFICIENCY, GENERATION, DEFENSE, BINDING, INNATE
Background: The hyper IgE syndrome (HIES) is characterized by abscesses, eczema, recurrent infections, skeletal and connective tissue abnormalities, elevated serum IgE, and diminished inflammatory responses. It exists as autosomal-dominant and autosomal-recessive forms that manifest common and distinguishing clinical features. A majority of those with autosomal-dominant HIES have heterozygous mutations in signal transducer and activator of transcription (STAT)-3 and impaired T(H)17 differentiation.