Daniel L. Mueller

Dr. Daniel Mueller is a Professor of Medicine, and Chief 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 member of the Autoimmunity Program, within the University 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-cell tolerance within the peripheral immune system.

Research being conducted by Dr. Daniel Mueller

Autoimmunity develops as the consequence of a loss of tolerance to self-antigens. Investigations carried out by Daniel Mueller are leading to a better understanding of the biological and biochemical nature of immune self-tolerance. Of particular interest have been those factors that determine whether 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. His long-term goal in this work is the translation of an increased understanding of peripheral tolerance into the development of clinical strategies designed to re-institute immune self-tolerance in individuals with autoimmune disease, thereby eliminating the requirement for long-term, non-specific, and potentially life-threatening immunosuppression in their management. Currently, experiments are examining the role of B7/CD28 costimulatory signals in the generation of signals leading to autocrine growth production and cell cycle progression. In particular, experiments are investigating the regulation of nuclear co-activator function by costimulatory signals. The role of the translation-initiation regulator mTOR and the ubiquinin-directed proteosomal degradation pathway in the prevention/reversal of the clonal anergy is being studied. Lastly, he is using a mouse model of autoimmune arthritis to test the capacity of clonal anergy induction to control aberrant T-cell responses. This research is supported by an NIH-sponsored research grant on which he is a principal investigator.

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