Dr. James Elder, Kirk D. Wuepper Professor of Molecular Genetic Dermatology, received his MD and PhD in Molecular Biophysics and Biochemistry from Yale University, followed by an Internal Medicine Internship and a Dermatology Residency and Fellowship at the University of Washington. He is board-certified in Dermatology. Following his residency, Dr. Elder completed a Senior Research Fellowship at the University of Michigan. Dr. Elder directs an active research laboratory, utilizing molecular biology and genetics tools to better understand psoriasis, atopic dermatitis, and other human skin diseases.

Dr. Elder’s laboratory has made seminal contributions in using genetic linkage and association techniques to identify genetic signals for psoriasis and psoriatic arthritis. In 2006, his laboratory identified HLA-C*0602 as the disease allele at PSORS1, the major psoriasis susceptibility locus in the major histocompatibility complex (MHC). His current efforts in this area are focused on identifying additional psoriasis susceptibility loci, both within and outside the MHC. In a recent meta-analysis of genome-wide association studies (GWAS) involving nearly half a million individuals, Elder’s team and many international colleagues identified 109 distinct psoriasis susceptibility loci, including 46 that have not been previously reported, with more than one independent signal at 27 of the non-MHC loci. In a separate study, Elder and colleagues identified 17 independent signals within the MHC itself, mainly focused on the structure and regulation of other MHC Class I genes.

Currently, Dr. Elder is leading a global GWAS meta-analysis of psoriasis involving over one million individuals. He and his colleagues are also in the final stages of a decade-long genetic and genomic study designed to identify the actual genes whose regulation is affected by psoriasis genetic signals. Involving 153 individuals (76 controls and 87 psoriatic cases), this study utilized fluorescence-activated cell sorting of peripheral blood mononuclear cells to purify myeloid dendritic cells and eight subsets of T-cells (CD4/CD8 X CLA positive CLA-negative x 0 or 24h of T-cel activation with anti-CD3 / anti CD28 beads), followed by ATAC-seq and RNA-seq of each fraction, along with dense genotyping of all 153 individuals. Their results reveal a psoriasis-relevant nexus between T-cell activation and expansion of T17-polarized skin-homing T-cells. They suggest that skin-homing T-cells retain a chromatin-embedded memory of their prior activation in the skin.