ILC3 deficiency and generalized ILC abnormalities in DOCK8-deficient patients

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

ALLERGY, vol.75, no.4, pp.921-933, 2020 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 75 Issue: 4
  • Publication Date: 2020
  • Doi Number: 10.1111/all.14081
  • Journal Name: ALLERGY
  • Journal Indexes: 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
  • Page Numbers: pp.921-933
  • Keywords: 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 University Affiliated: Yes

Abstract

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.