Abstract：
:Mutations in the signal transducer and activator of transcription 3 (STAT3) were reported to cause hyperimmunoglobulin E syndrome (HIES). The present study investigates T helper type 17 (Th17) responses triggered by the relevant stimuli Staphylococcus aureus and Candidia albicans in five 'classical' HIES patients, and a family with three patients who all had a milder HIES phenotype. We demonstrate that patients with various forms of HIES have different defects in their Th17 response to S. aureus and C. albicans, and this is in line with the clinical features of the disease. Interestingly, a partial deficiency of interleukin (IL)-17 production, even when associated with STAT3 mutations, leads to a milder clinical phenotype. We also observed defective Th17 responses in patients with the 'classical' presentation of the disease but without STAT3 mutations. These data demonstrate that defective IL-17 production in response to specific pathogens can differ between patients with HIES and that the extent of the defective Th17 response determines their clinical phenotype.
journal_name
Clin Exp Immunoljournal_title
Clinical and experimental immunologyauthors
van de Veerdonk FL,Marijnissen RJ,Joosten LA,Kullberg BJ,Drenth JP,Netea MG,van der Meer JWdoi
10.1111/j.1365-2249.2009.04043.xsubject
Has Abstractpub_date
2010-01-01 00:00:00pages
57-64issue
1eissn
0009-9104issn
1365-2249pii
CEI4043journal_volume
159pub_type
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doi：
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doi：
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journal_title：Clinical and experimental immunology
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