We have demonstrated how mutations in multiple genes, including CD40L, TACI, MALT1, TFRC, and LRRC8A, result in impaired host immunity. Dr. Geha spearheads an international consortium of physicians and scientists committed to the diagnosis and treatment of patients with PIDs. By integrating genomic techniques, functional immunologic assays, and murine models of human disease, the lab has identified novel genetic causes of PIDs and elucidates the mechanisms underlying these diseases.
2. Mechanisms underlying allergic skin Inflammation, eczema vaccinatum (EV) and food allergy in atopic dermatitis (AD). AD is an allergic skin inflammation of the skin that affects more than 20% of children. The lab established a mouse model of AD elicited by epicutaneous (EC) sensitization that shares several key immunologic, histological and clinical features with AD, including the development of airway reactivity in response to inhaled antigen inhalation, the first experimental demonstration of the atopic march. This model has now been adapted by a number of laboratories for the study of the pathogenesis of AD. Using this model, we have elucidated the role of mechanical skin injury, skin innate immune cells, cytokines, transcription factors, chemokines, and eicosanoids in the development of AD. We have established murine models for EV and demonstrated that the cytokine IL-17A promotes vaccinia virus growth and IL-17A neutralization protects from EV. Our studies have had important implications for the understanding, prevention, and treatment of AD.
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