Dr. Ivashkiv joined the faculty of Hospital for Special Surgery and Weill Cornell Medical College in 1992, where he is currently Chief Scientific Officer (HSS) and Professor of Medicine and Immunology. His laboratory studies cytokine-mediated pathogenic mechanisms in autoimmune, inflammatory and musculoskeletal diseases. He focuses on regulation of cytokine signaling, cytokine production, gene transcription, and epigenomic regulation of the inflammatory phenotype of myeloid cells, osteoclasts and synovial fibroblasts that are important in pathogenesis of rheumatoid arthritis, inflammatory osteolysis and systemic lupus erythematosus. His studies have expanded our understanding of cytokine Jak-STAT signaling and its role in RA, mechanisms of inflammatory bone resorption and how they can be therapeutically targeted, the sustained inflammatory phenotype of synovial fibroblasts that contributes to unremitting inflammation, cellular responses to TNF and IFNs, and epigenomic regulation of the inflammatory response and how epigenetic mechanisms can be therapeutically targeted.

 Additional areas of interest include mechanisms that sustain inflammatory responses, functional coupling between macrophages and fibroblasts, transcription factor networks that control osteoclast differentiation and pathologic bone resorption, inflammatory modulation of stem cells in tissue repair, and using a transgenic approach that couples bacterial artificial chromosomes (BACs) and CRISPR-Cas9 genome editing to study the regulation of human autoimmunity-associated genes such as A20/TNFAIP3.

The laboratory integrates basic science investigation of signaling and epigenetic mechanisms with translational research using disease models and analysis of human disease samples with genome wide approaches such as RNA-seq, ChIP-seq, and ATAC-seq. We are incorporating a precision medicine approach to identify disease mechanisms and the best therapies for individual patients. Our long term goals are to identify signaling and epigenetic mechanisms that can be targeted by new therapies for inflammatory and autoimmune diseases.