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In 2008, Milner and colleagues [ 87 ] demonstrated that T cells in subjects with AD-HIES failed to produce interleukin (IL)-17 (but not interferon gamma) after mitogenic stimulation with staphylococcal enterotoxin B or after antigenic stimulation with Candida albicans or streptokinase. Purified naïve T cells were unable to differentiate into IL-17 producing the T helper (Th17) cells in vitro and had a lower expression of the retinoid-related orphan receptor (ROR)-γt, which is consistent with the crucial role of STAT3 signaling in the generation of Th17 cells. These Th17 cells have emerged as an important subset of helper T cells being critical in the clearance of fungal and extracellular bacterial infections. The Th17 cytokines, IL-17 (IL-17A) and IL-17F form biologically active homo- or heterodimers. Il-17 initiates nuclear factor kappa B (NF-κB) activation, leading to the transcription of multiple target genes involved in innate immunity. These include chemokines, such as CXCL8 (IL-8) and CCL20, the cytokines IL-6, tumor necrosis factor alpha (TNF-α), granulocyte- and granulocyte-macrophage colony-stimulating factor (G-CSF and GM-CSF, respectively), acute phase proteins such as C-reactive protein, antimicrobial peptides and mucins [ 88 ]. Thus, IL-17 plays an important role in antimicrobial defenses by recruiting and expanding the neutrophil lineage and producing antimicrobial peptides. The proinflammatory cytokines produced by Th17 cells include TNFα, IL-22 and IL-26, which are involved in innate immunity, and IL-6 which directs CD4+T cells differentiation towards the Th17 lineage. IL-22 has been associated with the generation of defensins, acute phase proteins and inflammatory cytokines [ 89 ]. This multidirectional, fundamental role of Th17 cells, including cells with specificities against candidal antigens explains the pattern of infection susceptibility characteristic of mutated HIES patients. In the recent report by Conti et al [ Womens Hanky Hem Dress EVANS Sast Online Online Cheap Authentic Footlocker Finishline Cheap Online zjYCN
] a decrease of salivary antimicrobial peptides, such as β-defensin 2 and Histatins has been demonstrated in AD-HIES patients, providing a mechanism for the severe susceptibility to oropharyngeal candidiasis. This finding supports this hypothesis of the crucial role of the Th17-dependent responses in immunity to .

Immune assessments of mutated AR-HIES patients reveal T cell lymphopenia with low counts of both CD4+ and CD8+ T cells, as well as impaired T cell expansion from activated peripheral blood mononuclear cells in vitro. In autosomal recessive HIES eosinophilia and the elevated serum IgE may be more pronounced than in AD-HIES []. In contrast to the latter syndrome, DOCK8 deficiency is associated with low IgM concentrations and impaired generation of a durable secondary antibody response to specific antigens, which accounts for the functional antibody abnormalities []. In a single patient with AR-HIES due to mutation, a normal number of lymphocytes was observed.

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