Lionel B IvashkivView profile
Professor
Lionel B Ivashkiv, MD , is Professor of Medicine and Immunology at Weill Cornell Medical College and Chief Scientific Officer at the Hospital for Special Surgery (HSS) , positions he has held since 1992. His dual affiliation places him at the forefront of translational research in autoimmune and inflammatory diseases. Education: MD, Harvard Medical School (1984) BA, Columbia University (1980) Research Focus: Dr. Ivashkiv's laboratory investigates cytokine-mediated pathogenesis in autoimmune, inflammatory, and musculoskeletal diseases. His work centers on the regulation of cytokine signaling, gene transcription, and epigenomic control of myeloid cells, osteoclasts, and synovial fibroblasts in diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and inflammatory osteolysis. He employs cutting-edge techniques including RNA-seq, ChIP-seq, ATAC-seq, and CRISPR-Cas9 genome editing to dissect molecular mechanisms and identify precision medicine approaches. Recent Trends in Publications: His recent work spans from epigenetic reprogramming of macrophages and monocytes to translational models of implant failure and fibrosis. Key themes include the interplay between TNF, IFN-γ, and IL-10 in shaping inflammatory responses, the role of epigenetic modifiers like EZH2 and KDM1A in osteoclastogenesis, and the development of computational tools for musculoskeletal pathology. Grants & Collaborations: Dr. Ivashkiv's research is supported by multiple NIH and foundation grants. He collaborates extensively with clinicians and engineers at HSS and Weill Cornell, and serves as a consultant to Eli Lilly and Company, translating his findings into therapeutic strategies for inflammatory diseases. Laboratory & Teams: His lab integrates basic science with translational medicine, working closely with orthopedic surgeons, rheumatologists, and bioinformaticians. The team focuses on identifying druggable targets in cytokine and epigenetic pathways to modulate inflammation and tissue damage in autoimmune diseases.









