Abstract Psoriatic Arthritis (PsA) is an immune mediated disease of the joint. It typically develops within 10 years after the onset of psoriasis, with ~30% of individuals progressing to joint disease. The progression of disease from skin to joint is not fully understood, although it is thought to be orchestrated by T helper 17 immune responses. To understand the immune landscape of PsA, we isolated immune cells from four matched PsA patient blood and synovium samples and performed multimodal single-cell sequencing (ExCITE-seq), which captures surface epitope information and T and B cell receptor rearrangement in addition to transcriptional profile. Our preliminary analysis revealed an enrichment of CD1c+/CD141+ dendritic cells (DCs) in synovium compared to the blood of PsA patients. Differential gene expression of these DC populations showed increased expression of CXCL16 in synovium derived DCs, while analysis of synovial fluid revealed high levels of CXCL10. Differential gene expression of CD8 and CD4 T cells across blood and synovium revealed increased granzyme K (GZMK) in the synovium. Further analyses comparing the GZMK+ T cell populations to their negative counterparts revealed upregulation of CXCR3, suggesting that CXCR3-CXCL10 axis may be responsible for recruitment and/or retention of T cells in the synovium. Pathway analysis for GZMK+ T cells revealed increased cytotoxicity and granulitic activity. Together this data suggests that GZMK+ T cells may contribute to inflammation in the joint of PsA patients, after recruitment to the site of inflammation by CD1c+/CD141+ DCs. Further characterization of additional PsA patients and psoriasis patients at risk for developing PsA is ongoing and will provide insight into PsA pathogenesis. Supported by a grant from the NIH (I&I Schwab T32) and funding from the National Psoriasis Foundation and the Colton Center for Autoimmunity.