{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T09:53:56Z","timestamp":1778579636124,"version":"3.51.4"},"reference-count":41,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2018,10,15]],"date-time":"2018-10-15T00:00:00Z","timestamp":1539561600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2019,2]]},"abstract":"Abstract<\/jats:title>Background<\/jats:title>Hyper\u2010IgE syndromes (HIES<\/jats:styled-content>) are a clinically overlapping, heterogeneous group of inborn errors of immunity characterized by elevated serum IgE level, eosinophilia, atopy, and immune dysregulation. Deficiency of DOCK<\/jats:styled-content>8 protein is potentially a life\u2010threatening autosomal recessive HIES<\/jats:styled-content> and only curable with bone marrow transplantation. Hence, the diagnosis of DOCK<\/jats:styled-content>8 deficiency is critical and should be sought at an early stage to initiate definitive therapy.<\/jats:p><\/jats:sec>Methods<\/jats:title>Serum samples from patients with DOCK<\/jats:styled-content>8 deficiency and atopic dermatitis were profiled on a cytokine\/chemokine panel for potential differential expression.<\/jats:p><\/jats:sec>Results<\/jats:title>CXCL<\/jats:styled-content>10 and TNF<\/jats:styled-content>\u2010A were upregulated in DOCK<\/jats:styled-content>8 patients when compared to AD<\/jats:styled-content>, possibly contributing toward increased susceptibility to infections and cancer. In contrast, epidermal growth factor (EGF<\/jats:styled-content>) was significantly downregulated in a subgroup of DOCK<\/jats:styled-content>8\u2010deficient and AD<\/jats:styled-content> patients, while IL<\/jats:styled-content>\u201031 expression was comparable between both DOCK<\/jats:styled-content>8\u2010deficient and AD<\/jats:styled-content> cohorts, possibly contributing toward pruritus seen in both groups.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>This comprehensive cytokine profile in HIES<\/jats:styled-content> patients reveals distinctive biomarkers that differentiate between the DOCK<\/jats:styled-content>8\u2010deficient and AD<\/jats:styled-content> patients. The unique expression profile of various inflammatory cytokines in patients with DOCK<\/jats:styled-content>8 deficiency vs atopic dermatitis likely reflects disease\u2010specific perturbations in multiple cellular processes and pathways leading to a predisposition to infections and allergies seen in these patients. These data agree with the role for EGF<\/jats:styled-content> replacement therapy in EGF<\/jats:styled-content>\u2010deficient individuals with AD<\/jats:styled-content> as well as DOCK<\/jats:styled-content>8 deficiency through a potential shared pathway. In addition, these novel biomarkers may be potentially useful in distinguishing DOCK<\/jats:styled-content>8 deficiency from AD<\/jats:styled-content> allowing early\u2010targeted treatment options.<\/jats:p><\/jats:sec>","DOI":"10.1111\/all.13610","type":"journal-article","created":{"date-parts":[[2018,9,25]],"date-time":"2018-09-25T15:52:51Z","timestamp":1537890771000},"page":"370-379","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Quantitative profiling of cytokines and chemokines in DOCK<\/scp>8\u2010deficient and atopic dermatitis patients"],"prefix":"10.1111","volume":"74","author":[{"given":"Minnie","family":"Jacob","sequence":"first","affiliation":[{"name":"Department of Genetics King Faisal Specialist Hospital and Research Centre (KFSHRC) Riyadh Saudi Arabia"},{"name":"College of Public Health, Medical and Veterinary Sciences Australian Institute of Tropical Health and Medicine James Cook University 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