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1 inactivating STAT3 mutations that result in hyper IgE syndrome.
2 Mutations in STAT3 cause autosomal dominant hyper-IgE syndrome.
3 inct clinical features of autosomal dominant hyper-IgE syndrome.
4 using localized candidiasis in patients with hyper-IgE syndrome.
5 AT3 in 50 familial and sporadic cases of the hyper-IgE syndrome.
6 h autoimmune disorders, or patients with the hyper-IgE syndrome.
7 ologic, dental, and skeletal features of the hyper-IgE syndrome.
8 the 27 relatives at risk for inheriting the hyper-IgE syndrome, 10 were fully affected, 11 were unaf
10 Nearly every patient with autosomal-dominant hyper-IgE syndrome (AD-HIES) due to signal transducer an
13 cells from patients with autosomal dominant hyper-IgE syndrome (AD-HIES) resist such EBV oncogene-dr
14 tion 3 (STAT3) mutations (autosomal dominant hyper-IgE syndrome [AD-HIES]) are partially protected fr
15 underlie sporadic and dominant forms of the hyper-IgE syndrome, an immunodeficiency syndrome involvi
16 disorders (found in 3 of 3 patients with the hyper-IgE syndrome and 4 of 7 patients with severe atopi
18 gitudinal clinical data on patients with the hyper-IgE syndrome and their families and assayed the le
20 and mononuclear cells from patients with the hyper-IgE syndrome, as compared with levels in control c
21 ation among patients with autosomal dominant hyper-IgE syndrome carrying heterozygous signal transduc
22 ciency with phenotypic similarities to STAT3 hyper-IgE syndrome caused by loss of function of GP130.
24 8) gene cause an autosomal recessive form of hyper-IgE syndrome, characterized by chronic immunodefic
25 eactions in patients with autosomal dominant hyper-IgE syndrome compared with that seen in atopic sub
26 n contrast, the cells from patients with the hyper-IgE syndrome generated lower levels of monocyte ch
33 severe atopic dermatitis (AD) overlaps with hyper-IgE syndromes (HIES) regarding eczema, eosinophili
37 cell, collagen, and goblet cell hyperplasia; hyper IgE syndrome; mucus plugging; and extensive induci
43 cells from patients with autosomal dominant hyper-IgE syndrome, which is caused by STAT3 deficiency,
44 mory B cells were described in patients with hyper-IgE syndrome, which is consistent with defective a
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