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Gurjit (Neeru) K. Khurana Hershey, MD, PhDProfessor and Director, Division of Asthma ResearchKindervelt Endowed Chair in Asthma ResearchDepartment of Pediatrics; Division of Asthma Research
Dr. Hershey investigates regulatory mechanisms of allergic inflammation. One major research focus is identification of epithelial genes and pathways that contribute to allergic inflammation and atopic disorders. Dr. Relevant to digestive disease research, Dr. Hershey utilizes custom Illumina SNP arrays to identify epithelial genes and pathways that are associated with atopic disorder phenotypes. Recently, she was awarded a grant to identify epithelial genes that are common and those genes that are distinct between the lung (asthma), gut (food allergy) and skin (atopic dermatitis). Testing of related hypotheses in the laboratory, Dr. Hershey began dissecting the molecular basis of allergic inflammation at these target organs and the unique and redundant epithelial pathways using in vitro and in vivo experimental models of disease.
Dr. Hershey collaborates with Drs. Aronow and Rothenberg on the grant Epithelial Genes in Allergic Inflammation. She also works with Drs. Aronow on several ongoing genomic and genetic studies, and with Dr. Jeffrey Whitsett on the role of serpins in mucus production. Anticipated use of Cores: Integrative Morphology and Gene and Protein Expression Cores.
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Associations of TSLP SNPs with eosinophilic esophagitis (EE) are independent of allergy phenotypes. Upper panel: The associated –log10 P values for the genotyped TSLP SNPs from each analysis (patients with EE vs allergic or nonallergic control subjects) are plotted based on relative base pair location. The dashed line represents the Bonferroni threshold for significance. In the lower panel, the TSLP SNPs reside within an approximate 8-kb interval on 5q22.1 encoding the TSLP gene isoforms. Represented are exons (white boxes), introns (bold lines), and untranslated regions (gray boxes). Figure from J Allergy Clin Immunol 2010;126;160-6.
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