Dept. of Pathology Faculty

R. Hal Scofield, M.D.

The University of Oklahoma
Health Sciences Center
Oklahoma Medical Research Foundation
825 N.E. 13th
Room B-207.1, Mail Box 38
Oklahoma City, Oklahoma 73104

PHONE: (405) 271-7061

Fax: (405)271-7063

E-MAIL: Hal-Scofield@omrf.ouhsc.edu

TITLES

Associate Member
Arthritis and Immunology Research Program
Oklahoma Medical Research Foundation

Adjunct Associate Professor,
Department of Pathology

Professor,
Department of Medicine

EDUCATION

Texas A&M University
B.A. (1980)

University of Texas Southwestern
Medical School
Dallas, TX
MD (1984)

memberships:

American College of Physicians
American College of Rheumatology
American Federation of Clinical Research
The Endocrine Society
American Association for the Advancement of Science
Oklahoma Rheumatism Association
The Society of General Internal Medicine
The New York Academy of Sciences
American Association of Immunologists

Research Interests/Sub-Specialty

Broadly, the charge of the immune system is to distinguish self from non-self. In autoimmune diseases, this ability fails, resulting in self-, or auto, immunity. My research concentrates on systemic autoimmune diseases, which are characterized by a loss of tolerance to self in the form of ubiquitously expressed antigens. Our approach calls upon a wide range of scientific disciplines, ranging from clinical research of particular patient populations to laboratory-based basic research to animal models of human disease. We are interested in spondyloarthropathies, such as ankylosing spondylitis, which are strongly associated with HLA-B27. We have identified a human immune response against HLA-B27 that is present on the cell surface in a conformation different from the usual one in which the HLA class I heavy chain is associated with short peptide and beta-2-microglobulin. Other studies are investigating cytokines expression in peripheral blood mononuclear cells from patients and controls. These studies demonstrate a unique profile for patients as well as HLA_B27-positive controls.

We are also interested in systemic lupus erythematosus and Sjögren's syndrome, both of which are characterized by autoantibodies binding the proteins of the Ro/La ribonucleoprotein particle. We have a long-standing interest in the structure of this particle and continue to pursue work to determine protein-protein interactions within the particle. We have shown that anti-Ro is involved in pathophysiology of neutropenia in lupus and Sjögren's patients and work continues on neutropenia in neonatal lupus. Another interest is immunization of animals with short peptides from 60 kD Ro, which induces epitope spreading as well as a Sjögren's syndrome-like illness in some mouse strains. The immunology and genetics of this model are being explored, including prevention by oral tolerance. Human lupus is being studied at the level of B cell immunity. We are exploring antibodies binding critical oxidative protection mechanisms, such as superoxide dismutase. This complements the animal immunization studies in that oxidatively modified antigens induce enhanced epitope spreading.

The genetics of lupus are being explored. In particular, we are studying a putative gene on chromosome 11 linked to severe lupus in black Americans. Studies are underway to pinpoint this genetic effect in a localized region of this chromosome.

PUBLICATIONS