Faculty ProfilesMickie Cheng, MD
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.
Recent Articles (10)
Watkin LB, Jessen B, Wiszniewski W, Vece TJ, Jan M, Sha Y, Thamsen M, Santos-Cortez RL, Lee K, Gambin T, Forbes LR, Law CS, Stray-Pedersen A, Cheng MH, Mace EM, Anderson MS, Liu D, Tang LF, Nicholas SK, Nahmod K, Makedonas G, Canter DL, Kwok PY, Hicks J, Jones KD, Penney S, Jhangiani SN, Rosenblum MD, Dell SD, Waterfield MR, Papa FR, Muzny DM, Zaitlen N, Leal SM, Gonzaga-Jauregui C, Boerwinkle E, Eissa NT, Gibbs RA, Lupski JR, Orange JS, Shum AK. COPA mutations impair ER-Golgi transport and cause hereditary autoimmune-mediated lung disease and arthritis. Nat Genet. 2015 Jun; 47(6):654-60.
Price JV, Haddon DJ, Kemmer D, Delepine G, Mandelbaum G, Jarrell JA, Gupta R, Balboni I, Chakravarty EF, Sokolove J, Shum AK, Anderson MS, Cheng MH, Robinson WH, Browne SK, Holland SM, Baechler EC, Utz PJ. Protein microarray analysis reveals BAFF-binding autoantibodies in systemic lupus erythematosus. J Clin Invest. 2013 Dec; 123(12):5135-45.
Shum AK, Alimohammadi M, Tan CL, Cheng MH, Metzger TC, Law CS, Lwin W, Perheentupa J, Bour-Jordan H, Carel JC, Husebye ES, De Luca F, Janson C, Sargur R, Dubois N, Kajosaari M, Wolters PJ, Chapman HA, Kämpe O, Anderson MS. BPIFB1 is a lung-specific autoantigen associated with interstitial lung disease. Sci Transl Med. 2013 Oct 09; 5(206):206ra139.
Cheng MH, Fan U, Grewal N, Barnes M, Mehta A, Taylor S, Husebye ES, Murphy EJ, Anderson MS. Acquired autoimmune polyglandular syndrome, thymoma, and an AIRE defect. N Engl J Med. 2010 Feb 25; 362(8):764-6.
Zhang L, Barker JM, Babu S, Su M, Stenerson M, Cheng M, Shum A, Zamir E, Badolato R, Law A, Eisenbarth GS, Anderson MS. A robust immunoassay for anti-interferon autoantibodies that is highly specific for patients with autoimmune polyglandular syndrome type 1. Clin Immunol. 2007 Nov; 125(2):131-7.