Lionel B. Ivashkiv, MD

Dr. Lionel B. Ivashkiv joined Hospital for Special Surgery staff in 1992. He combines clinical care of patients with arthritis and inflammatory diseases with basic research in inflammation and gene regulation. Dr. Ivashkiv serves as head of the Rheumatoid Arthritis Registry. He is the Director of the HSS Genomics Center which was established with a $5.6 million grant from The Tow Foundation to study rheumatoid athritis and lupus.

Appointments

Attending Physician, Hospital for Special Surgery
Associate Chief Scientific Officer, Hospital for Special Surgery
David H. Koch Chair in Arthritis and Tissue Degeneration
Professor, Medicine and Immunology, Weill Cornell Medical College
Director, HSS Genomics Center

Specialty

Special Expertise

Rheumatoid arthritis
Inflammatory bone diseases

Awards

Jack Friedman Young Investigator Prize, Weill Cornell Medical College, 1995
Young Scholar Award, Arthritis Foundation, New York Chapter, 1995
Arthritis Investigator Award, 1993
Clinical Investigator Award, 1990
Soma Weiss Award, Harvard Medical School, 1984

Specialized Centers

Education

MD, Harvard Medical School, Cambridge, Massachusetts

Residency

New York University - Bellevue Hospital, New York

Fellowship

Harvard Medical School - Brigham and Women's Hospital

Certification

Rheumatology
Internal Medicine

State Licensure

New York

Lionel B. Ivashkiv, MD has contributed to the following articles on HSS.edu:

Selected Publications

Ivashkiv, L. B.  2008. A signal switch hypothesis for cross-regulation of cytokine and TLR signalling pathways. Nature Rev. Immunology. 8:816-822. NIHMSID #72160

 Hu, X., A. Chung, I. Wu, J. Foldi, J. Chen, J.-D.Ji, T. Tateya, Y. J. Kang, J. Han, M. Gessler, R. Kageyama and L. B. Ivashkiv. 2008. Selective and Reciprocal Regulation of TLR-inducible Gene Subsets by Notch and IFN-g Pathways. Immunity. 29:691-703. NIHMSID # 77245

 Hu, X., S. D. Chakravarty and L. B. Ivashkiv. 2008. Regulation of IFN and TLR signaling during macrophage activation by opposing feedforward and feedback inhibition mechanisms. Immunol. Rev. (In Press). NIHMSID #71125

For more publications, please see the PubMed listing.

Research Description

Cytokine Signaling and Inflammation

Cytokines are secreted proteins that mediate communication between cells. Cytokines trigger signal transduction and gene activation cascades that regulate cellular activation, proliferation, differentiation, and survival. A critical role for cytokines in immunity and inflammation, and in arthritis and autoimmune diseases, is now well established. New biological therapies aimed at neutralizing cytokines have been very successful and have initiated a new era of rational therapy of inflammatory and autoimmune diseases.

Our laboratory studies a major signal transduction pathway utilized by many cytokines, the Janus kinase ¡V signal transducer and activator of transcription (Jak-STAT) pathway. The laboratory is characterizing molecular mechanisms that regulate signaling by the Jak-STAT pathway. We are developing the idea that modulation or reprogramming of cytokine signaling during inflammation is an important determinant of the balance of cytokine action. We are studying the mechanisms and the impact of modulation of cytokine signaling on cell function and gene expression, and on the severity of inflammation and related tissue damage. For example, we have shown that signaling by the anti-inflammatory cytokine interleukin-10 (IL-10) is suppressed in rheumatoid arthritis (RA), such that IL-10 is no longer active. In systemic lupus erythematosus (SLE), IL-10 signaling is reprogrammed such that IL-10 acquires pro-inflammatory functions and thus contributes to inflammation instead of suppressing it. A new area of investigation in our laboratory is the analysis of cytokine regulation of tissue destruction and remodeling.

The laboratory takes an integrated bench to bedside approach and studies signal transduction defects in human disease samples, in defined in vitro systems, and in animal models of arthritis and SLE. Biochemical approaches are complemented by genetic approaches that utilize RNA interference or knockout mice, and by microarray analysis of genome-wide gene expression. The long term goals of our laboratory are to define the molecular basis of the regulation of cytokine signaling during inflammation, and to target signaling pathways as a novel approach to therapy.

Clinical Trials

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