Atıf İçin Kopyala
ENGELHARDT K. R., GERTZ M. E., KELES S., SCHAEFFER A. A., SIGMUND E. C., GLOCKER C., ...Daha Fazla
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, cilt.136, sa.2, ss.402-412, 2015 (SCI-Expanded)
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Yayın Türü:
Makale / Tam Makale
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Cilt numarası:
136
Sayı:
2
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Basım Tarihi:
2015
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Doi Numarası:
10.1016/j.jaci.2014.12.1945
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Dergi Adı:
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
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Derginin Tarandığı İndeksler:
Science Citation Index Expanded (SCI-EXPANDED), Scopus
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Sayfa Sayıları:
ss.402-412
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Anahtar Kelimeler:
Primary combined immunodeficiency, hyper-IgE syndrome, autosomal recessive hyper-IgE syndrome, dedicator of cytokinesis 8, signal transducer and activator of transcription 3, Molluscum contagiosum, HYPER-IGE SYNDROME, BONE-MARROW-TRANSPLANTATION, STEM-CELL TRANSPLANTATION, DOCK8 DEFICIENCY, MUTATIONS, IMMUNODEFICIENCY, STAT3, GLYCOSYLATION, DISORDER, SURVIVAL
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Erciyes Üniversitesi Adresli:
Evet
Özet
Background: Mutations in dedicator of cytokinesis 8 (DOCK8) cause a combined immunodeficiency (CID) also classified as autosomal recessive (AR) hyper-IgE syndrome (HIES). Recognizing patients with CID/HIES is of clinical importance because of the difference in prognosis and management.