Rheumatology & Clinical Immunology
Rheumatology and Clinical Immunology Faculty
Eric S. Sobel, M.D., Ph.D.
Associate Professor
B.S. Chemistry University of Toledo, 1977
Ph.D. Biochemistry Case Western Reserve University, 1983
M.D. Medicine Case Western Reserve University, 1984
Professional Information
- Residency (Internal Medicine): University of North Carolina Hospitals 1984-1987
- Fellowship: (Rheumatology) University of North Carolina Hospitals 1987-1990
- Clinical Instructor University of North Carolina at Chapel Hill 1990-1992
- Research Assistant Professor University of North Carolina at Chapel Hill 1992-1993
Editorial Boards:
- Editorial Board, Clinical Immunology, 1996-2001.
- Associate Editor, Journal of Immunology, 1995-present.
- Arthritis and Rheumatism ad hoc reviewer 1999-present
Advisory Panels:
- Reviewer for National American Heart Association, 1999-2001.
- Ad hoc reviewer for NIH GMA-1 study section.
- Reviewer for NIH Special Emphasis Panel, June 2000.
- Reviewer for NIH Special Emphasis Panel, April 2001
- Reviewer for Oklahoma Center for the Advancement of Science and Technology, 1994, 1997-2000.
- Reviewer of abstracts, Annual Scientific Meeting of the American College of Rheumatology, 1994, 1997, and 2001.
- The Henry Kunkel Society
Research interest:
Mouse models of systemic autoimmunity
Clinical interests:
Systemic lupus erythematosus, rheumatoid arthritis, polymyositis, and scleroderma
Research Description
Our laboratory is interested in murine models of autoimmune disease, both spontaneous and induced. We have two major projects. The first uses mercury chloride to induce an anti-nucleolar response in certain strains of mice. This response is directed to fibrillarin, a ribosomal RNA processing protein and is a specificity most commonly found in systemic sclerosis (scleroderma). We are examining the cellular interactions leading to this response.
In the second major project, we are collaborating with Dr. Edward Wakeland and Dr. Laurence Morel in the complex genetic inheritance of lupus in the NZM/2410 mice, which were derived from the classic (NZBxNZW)F1 model. Genetic intervals have been identified and individually backcrossed onto non-autoimmune strains of mice. Through bone marrow transplant experiments, we are exploring how these genes are expressed and delineating the immunological pathways they affect. The overall goal is to identify genes leading to a break in tolerance to self-antigen.
Representative Publications
Sobel ES, Kakkanaiah M, Cohen PL, and Eisenberg RA. Co-infusion of normal bone marrow partially corrects the gld T-cell defect. Evidence for an intrinsic and extrinsic role for Fas ligand. J. Immunol. 154(1): 459-464, 1995.
Hanley GA., Schiffenbauer J, and Sobel ES.. Class II haplotype differentially regulates immune response in HgCl2-treated mice. Clin. Immunol. Immunopathol., 84:328-37, 1997.
Hanley, G.A., Schiffenbauer J., and Sobel E.S. Resistance to HgCl2-induced autoimmunity in haplotype-heterozygous mice is an intrinsic property of B cells. J. Immunol. 161:1778-1785. 1998.
Sobel ES, Mohan C, Morel L, Schiffenbauer J, and Wakeland E K.. Genetic dissection of SLE pathogenesis: adoptive transfer of Sle1 mediates the loss of tolerance by bone-marrow-derived B cells. J. Immunol. 162: 2415-2421, 1999
Khaled, A.R., Butfiloski, E.J., Villas B., Sobel, E.S., and Schiffenbauer, J. Aberrant expression of the NK-κB and IκB proteins in B cells from viable motheaten mice. Autoimmun. 30:115-128, 1999.