Betty Diamond
Betty Diamond received an MD from Harvard Medical School in 1973. She performed a residency in Internal Medicine at Columbia Presbyterian Medical Center, and then a post-doctoral fellowship in Immunology with Dr. Matthew Scharff at the Albert Einstein College of Medicine. She is currently Head of the Autoimmune Disease Center at the Feinstein Institute for Medical Research, and on the faculty of the Albert Einstein College of Medicine.
Dr Diamond’s research has focused on the induction and pathogenicity of anti-DNA antibodies in Systemic Lupus Erythematosus. She received the Outstanding Investigator Award of the ACR in 2001, the Lee Howley Award from the Arthritis Foundation in 2002, and the Recognition Award from the National Association of MD-PhD Programs in 2004 and was elected to the Institute of Medicine in 2006. Dr. Diamond is on the Scientific Council of NIAMS and the Board of Directors of the American College of Rheumatology.
Dr. Diamond’s primary interests are in the mechanisms of central and peripheral tolerance of autoreactive B cells, and the defects in these mechanisms that are present in autoimmune disease. Her laboratory has been studying the regulation of DNA-reactive B cells and the role of hormones and antigen in inducing autoimmunity. In a mouse transgenic for the heavy chain of a pathogenic anti-DNA antibody, elevated concentrations of both estradiol and prolactin break tolerance, cause high affinity anti-DNA B cells that are normally deleted in the bone marrow to be activated and contribute to the expressed antibody repertoire. Studies have shown that each hormone affects different pathways in B cell development.
Dr. Diamond’s laboratory has also developed a model of SLE induced by immunization with a peptide mimetope of DNA. This model is of interest because it demonstrates that pathogenic autoreactivity can be induced in a non-spontaneously autoimmune host. Furthermore, mouse strains differ in their susceptibility to this antigen-induced model of SLE. The laboratory has performed genetic analyses to identify 3 chromosomal loci in BALB/c mice important in conferring disease susceptibility.
Finally, Dr. Diamond’s laboratory has demonstrated that a subset of anti-DNA antibodies cross-reacts with the NMDA receptor. These antibodies can mediate neuronal apoptosis in the hippocampus leading to a memory deficit or in the amygdala leading to a behavioral alteration. These studies show that lupus antibodies can cause aspects of neuropsychiatric lupus in a non-inflammatory fashion and create a paradigm for antibody-mediated changes in brain function in many conditions.
