ILC3 deficiency and generalized ILC abnormalities in DOCK8-deficient patients

Eken, AHMET; Cansever, Murat; Okus, Fatma; Erdem, Serife; Nain, Ercan; Azizoglu, Zehra; Haliloglu, Yesim; Karakukcu, MUSA; Ozcan, ALPER; Devecioglu, Omer; Aksu, Guzide; Arikan Ayyildiz, Zeynep; Topal, Erdem; Karakoc Aydiner, Elif; Kiykim, Ayca; Metin, Ayse; Cipe, Funda; Kaya, Aysenur; Artac, Hasibe; Reisli, Ismail; Guner, Sukru; Uygun, Vedat; Karasu, Gulsun; Dönmez Altuntas, HAMİYET; Canatan, Halit; Oukka, Mohamed; Ozen, Ahmet; Chatila, Talal; Keles, Sevgi; Baris, Safa; Unal, EKREM; Patiroglu, Turkan

doi:10.1111/all.14081

ILC3 deficiency and generalized ILC abnormalities in DOCK8-deficient patients

Atıf İçin Kopyala

Eken A., Cansever M., Okus F. Z., Erdem S., Nain E., Azizoglu Z. B., ...Daha Fazla

ALLERGY, cilt.75, sa.4, ss.921-933, 2020 (SCI-Expanded)

Yayın Türü: Makale / Tam Makale
Cilt numarası: 75 Sayı: 4
Basım Tarihi: 2020
Doi Numarası: 10.1111/all.14081
Dergi Adı: ALLERGY
Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Agricultural & Environmental Science Database, BIOSIS, CAB Abstracts, EMBASE, Food Science & Technology Abstracts, MEDLINE, Veterinary Science Database
Sayfa Sayıları: ss.921-933
Anahtar Kelimeler: DOCK8, Hyper-IgE syndrome (HIES), ILC, ILC3, STAT3, INNATE LYMPHOID-CELLS, ROR-GAMMA-T, IMMUNE-DEFICIENCY, IL-7 RECEPTOR, DOCK8, MUTATIONS, DEDICATOR, EXPRESSION, IMMUNODEFICIENCY, GLYCOSYLATION
Erciyes Üniversitesi Adresli: Evet

Özet

BackgroundDedicator of cytokinesis 8 (DOCK8) deficiency is the main cause of the autosomal recessive hyper-IgE syndrome (HIES). We previously reported the selective loss of group 3 innate lymphoid cell (ILC) number and function in a Dock8-deficient mouse model. In this study, we sought to test whether DOCK8 is required for the function and maintenance of ILC subsets in humans.