DOCK8 Deficiency Exacerbates Skin Contact Hypersensitivity

Contact Hypersensitivity CXCR3 Deficiency Prolongs Th1-Type

Clinical aspects of contact hypersensitivity

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Cutaneous manifestations of DOCK8 deficiency syndrome.

BACKGROUND Mutations in the dedicator of cytokinesis 8 gene (DOCK8) cause a combined primary immunodeficiency syndrome that is characterized by elevated serum IgE levels, depressed IgM levels, eosinophilia, sinopulmonary infections, cutaneous viral infections, and lymphopenia. Many patients with DOCK8 deficiency were previously thought to have a variant of Job's syndrome. Distinguishing between...

The transcription factor EPAS1 links DOCK8 deficiency to atopic skin inflammation via IL-31 induction

Mutations of DOCK8 in humans cause a combined immunodeficiency characterized by atopic dermatitis with high serum IgE levels. However, the molecular link between DOCK8 deficiency and atopic skin inflammation is unknown. Here we show that CD4+ T cells from DOCK8-deficient mice produce large amounts of IL-31, a major pruritogen associated with atopic dermatitis. IL-31 induction critically depends...

ONZIN Deficiency Attenuates Contact Hypersensitivity Responses in Mice

ONZIN is abundantly expressed in immune cells of both the myeloid and lymphoid lineage. Expression by lymphoid cells has been reported to further increase after cutaneous exposure of mice to antigens and haptens capable of inducing contact hypersensitivity (CHS), suggesting that ONZIN has a critical role in this response. Here, we report that indeed ONZIN-deficient mice develop attenuated CHS t...