{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T16:50:35Z","timestamp":1790009435838,"version":"4.0.1"},"reference-count":57,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2019,10,31]],"date-time":"2019-10-31T00:00:00Z","timestamp":1572480000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003062","name":"Erciyes \u00dcniversitesi","doi-asserted-by":"publisher","award":["TOA\u20102016\u20106130"],"award-info":[{"award-number":["TOA\u20102016\u20106130"]}],"id":[{"id":"10.13039\/501100003062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000098","name":"NIH Clinical Center","doi-asserted-by":"publisher","award":["5R01AI085090, 5R01AI128976"],"award-info":[{"award-number":["5R01AI085090, 5R01AI128976"]}],"id":[{"id":"10.13039\/100000098","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2020,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Dedicator of cytokinesis 8 (DOCK8) deficiency is the main cause of the autosomal recessive hyper\u2010IgE syndrome (HIES). We previously reported the selective loss of group 3 innate lymphoid cell (ILC) number and function in a\n                      <jats:italic>Dock8<\/jats:italic>\n                      \u2010deficient mouse model. In this study, we sought to test whether DOCK8 is required for the function and maintenance of ILC subsets in humans.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Peripheral blood ILC1\u20103 subsets of 16 DOCK8\u2010deficient patients recruited at the pretransplant stage, and seven patients with autosomal dominant (AD) HIES due to STAT3 mutations, were compared with those of healthy controls or post\u2010transplant DOCK8\u2010deficient patients (n\u00a0=\u00a012) by flow cytometry and real\u2010time qPCR. Sorted total ILCs from DOCK8\u2010 or STAT3\u2010mutant patients and healthy controls were assayed for survival, apoptosis, proliferation, and activation by IL\u20107, IL\u201023, and IL\u201012 by cell culture, flow cytometry, and phospho\u2010flow assays.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>DOCK8\u2010deficient but not STAT3\u2010mutant patients exhibited a profound depletion of ILC3s, and to a lesser extent ILC2s, in their peripheral blood. DOCK8\u2010deficient ILC1\u20103 subsets had defective proliferation, expressed lower levels of IL\u20107R, responded less to IL\u20107, IL\u201012, or IL\u201023 cytokines, and were more prone to apoptosis compared with those of healthy controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>DOCK8 regulates human ILC3 expansion and survival, and more globally ILC cytokine signaling and proliferation. DOCK8 deficiency leads to loss of ILC3 from peripheral blood. ILC3 deficiency may contribute to the susceptibility of DOCK8\u2010deficient patients to infections.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/all.14081","type":"journal-article","created":{"date-parts":[[2019,10,9]],"date-time":"2019-10-09T10:09:22Z","timestamp":1570615762000},"page":"921-932","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["ILC3 deficiency and generalized ILC abnormalities in DOCK8\u2010deficient patients"],"prefix":"10.1111","volume":"75","author":[{"given":"Ahmet","family":"Eken","sequence":"first","affiliation":[{"name":"Department of Medical Biology Erciyes University School of Medicine Kayseri Turkey"},{"name":"Bet\u00fcl\u2010Ziya Eren Genome and Stem Cell Center (GENKOK) Kayseri Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Murat","family":"Cansever","sequence":"additional","affiliation":[{"name":"Departments of Pediatrics Division of Pediatric 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