Assistant Professor
Assistant Professor of Pediatrics
+1 415 502-9581
+1 415 502-7540

Biography

Autoimmune disease affects up to 5% of the population and can cause significant morbidity and mortality. Our labs main focus is to understand the basic mechanisms by which immune tolerance is broken in order to identify novel therapeutic targets for the treatment of autoimmune diseases. We utilize a variety of mouse models to study both central tolerance and peripheral tolerance. Central tolerance is the process by which autoreactive T cells are deleted in the thymus through negative selection. We are currently utilizing a variety of novel conditional knockout mice to study the roles of specific proteins in thymic tolerance.

A second area of active research in the lab is the role of effector T cells in autoimmune disease. One subtype of CD4+ effector T cell, termed T helper 17 (Th17) cells have been found to be important in the pathogenesis of multiple autoimmune diseases and Th17 cells have been targeted therapeutically for treatment. We have identified the activating transcription factor 7 interacting protein (ATF7ip) as a novel regulator of Th17 cell differentiation and are currently studying its mechanism of action in Th17 cells and other immune cells.

Education and Training

Fellowship, 06/2011 Pediatric Rheumatology, University of California, San Francisco
Residency, 06/2008 Pediatrics, University of California, San Francisco
MD/PhD, 06/2005 Medicine, Penn State College of Medicine

Publications

Tsui JL, Estrada OA, Deng Z, Wang KM, Law CS, Elicker BM, Jones KD, Dell SD, Gudmundsson G, Hansdottir S, Helfgott SM, Volpi S, Gattorno M, Waterfield MR, Chan AY, Chung SA, Ley B, Shum AK. Analysis of pulmonary features and treatment approaches in the COPA syndrome. ERJ Open Res. 2018 Apr; 4(2).
LaFlam TN, Seumois G, Miller CN, Lwin W, Fasano KJ, Waterfield M, Proekt I, Vijayanand P, Anderson MS. Identification of a novel cis-regulatory element essential for immune tolerance. J Exp Med. 2015 Nov 16; 212(12):1993-2002.
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.
Waterfield M, Khan IS, Cortez JT, Fan U, Metzger T, Greer A, Fasano K, Martinez-Llordella M, Pollack JL, Erle DJ, Su M, Anderson MS. The transcriptional regulator Aire coopts the repressive ATF7ip-MBD1 complex for the induction of immunotolerance. Nat Immunol. 2014 Mar; 15(3):258-65.
Waterfield M, Anderson MS. Autoimmunity's collateral damage: Immunodeficiency hints at autoreactivity to cytokines. Nat Med. 2011 Sep 07; 17(9):1054-5.
Waterfield M, Anderson MS. Clues to immune tolerance: the monogenic autoimmune syndromes. Ann N Y Acad Sci. 2010 Dec; 1214:138-55.
Waterfield MR, Zhang M, Norman LP, Sun SC. NF-kappaB1/p105 regulates lipopolysaccharide-stimulated MAP kinase signaling by governing the stability and function of the Tpl2 kinase. Mol Cell. 2003 Mar; 11(3):685-94.