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Director of Rheumatic and Autoimmune Diseases
Department of Medicine
University of Wisconsin - Madison, 1983, M.D.
612-625-8477 - office
612-625-8614 - lab
Dr. Daniel Mueller is a Professor of Medicine, and Director of Rheumatic and Autoimmune Diseases at the University of Minnesota Medical School. He undertook his medical studies at the University of Wisconsin-Madison School of Medicine, and later obtained his Internal Medicine training at the Ohio State University Hospital. In 1986, he received training in basic molecular immunology in the Laboratory of Immunology at the National Institute for Allergy and Infectious Disease, NIH, under Drs. Ronald Schwartz and William Paul. It is there that he initiated his research into fundamental mechanisms involved in the development and maintenance of immune self-tolerance. In 1990, Dr. Mueller entered the Rheumatology Training Program in the Rheumatic Diseases Division/Department of Internal Medicine at the University of Texas Southwestern Medical Center, under Dr. Peter Lipsky. Since the completion of his medical and research training, he has been on the University of Minnesota Medical School faculty. He is also a Director of the Autoimmunity Program, within the Medical School’s Center for Immunology. The major focus of his academic program is the investigation of the biological and biochemical mechanisms that underlie the maintenance of T- and B-cell tolerance within the peripheral immune system.
Current Research being conducted:
Autoimmunity develops as the consequence of a loss of tolerance to self-antigens. Investigations carried out by Dr. Daniel Mueller are leading to a better understanding of the biological and biochemical nature of immune self-tolerance. Of particular interest are those factors that determine whether prolonged and continuous antigen stimulation of a T-cell will lead to an increase in the clone size and the development of protective (or pathological) effector function, or lead to its functional inactivation (clonal anergy) and T-cell tolerance. Chronic antigen recognition in the absence of costimulatory ligands normally leads to clonal anergy induction, rather than aggressive immunity. This does not appear to be true, however, for individuals who are deficient in Foxp3+ T regulatory cells, where antigen recognition invariably leads to an expansion of the clone, continued functional responsiveness, and in some case immunopathology. Loss of T cell tolerance also leads to the expansion and differentiation of autoreactive B cells, and the development of B-dependent autoimmune disease. Currently, these biological principles are being investigated in models of CD4+ T cell-mediated immunopathology using both monoclonal KRN TCR-transgenic mice, as well as self antigen-specific polyclonal responder T cells from normal mice. Finally, translational experiments are underway that investigate the repertoire of human autoreactive B cells in normals as well as in patients with Rheumatoid Arthritis and Systemic Lupus Erythematosus.