Mickie Cheng, MD
|School||UCSF School of Medicine|
|Address||513 Parnassus Ave|
San Francisco CA 94143
|University of Texas Southwestern||M.D.||2002||School of Medicine|
My research interests have been guided by a longstanding interest in genetics and developmental biology with a focus on reproductive biology. My training in endocrinology has introduced me to the unique intersection of these interests with immunology in the study of endocrine autoimmunity. The shift to research in immunology represents a new field of training which will enhance my distinct interests. My current research centers on investigations on autoimmune ovarian disease (AOD) by utilizing a novel mouse model of spontaneous autoimmune disease, the aire knockout mouse. AOD is a poorly understood condition leading to premature menopause and infertility in ~1.5 million women in the US. The focus of my work includes:
• Characterization of immune-mediated disease mechanisms leading to oophoritis
• Identification of a disease-specific ovarian antigen
• Study of mechanisms of antigen-specific tolerance induction
• Potential application of improved autoantibody screening to patients affected by premature ovarian failure
• Translation of antigenic targets from the animal model to improve diagnostic testing and identify therapeutic targets in human ovarian failure and infertility.
The identification of autoantibodies and target antigens in a mouse model will allow better elucidation of the steps that lead to the breakdown of immunologic tolerance in the ovary and thus disease pathogenesis. These targets may be shared with patients with AOD since the aire knockout mouse is a model for the known human autoimmune syndrome, APS 1. Identification of such targets will allow for potential translation of autoantibody testing for improved diagnosis of AOD patients and experiments to induce tolerance to putative shared antigens between the human and mouse model. Through the study of endocrine autoimmunity and its effect on reproductive biology, I plan to continue to address questions in the basic mechanisms of immune tolerance induction that will likely be shared among many different autoimmune diseases.
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