In July 2017, I joined Pfizer to lead the Discovery effort in the Inflammation and Immunology Research Unit at Pfizer located in Cambridge, MA. Prior to joining Pfizer, I was a Senior Investigator and Chief of the Immunopathogenesis Section of the Laboratory of Parasitic Disease, in the National Institute of Allergy and Infectious Diseases, NIH in Bethesda, MD. I received my Ph.D. from the Department of Medical Microbiology and Immunology at the University of Wisconsin, in Madison, Wisconsin. I have published over 200 research papers, reviews, and book chapters in many prestigious journals including Nature, Science, and Nature Immunology and have made important contributions to our understanding of the role of cytokines and growth factors in the progression and resolution of chronic inflammation, tissue regeneration, and fibrosis. At Pfizer, I’m leading our discovery efforts in the areas of immune tolerance, epithelial cell biology, immunometabolism, innate immunity, and fibrosis. For the past three years, I have been included on Thomson Reuters’ list of Highly Cited Researchers.

RESEARCH AREA(S)

The discovery group in the Inflammation and Immunology Research Unit focuses on core mechanisms that drive tissue damaging inflammation in important rheumatic, gastrointestinal, and dermatological diseases, including rheumatoid arthritis, systemic lupus erythematosus, ulcerative colitis, Crohn’s disease, non-alcoholic steatohepatitis, fibrosis, psoriasis, atopic dermatitis, alopecia, and vitiligo. Our work on immune tolerance is focused on identifying novel strategies to induce durable disease remission by harnessing endogenous regulatory mechanisms including immunosuppressive T cells. Epithelial cells have emerged as key drivers of several important chronic inflammatory diseases including atopic dermatitis, psoriasis, and IBD.

The epithelial biology group is using novel human cell based assays to better understand the role of the epithelium in disease pathogenesis and to test new therapeutics. The innate immunity is group is focused on understanding the role of danger sensing mechanisms and checkpoint (co-regulatory) receptor pathways in the initiation and maintenance of tissue damaging inflammatory responses. Similarly, the immunometabolism group is developing unique strategies to target metabolic pathways in important immune cells such as T cells and macrophages to restore immune homeostasis. Finally, the fibrosis groups is elucidating mechanisms that transform fat accumulation in the liver (steatosis) into a chronic inflammatory response (steatohepatitis) that can lead to fibrosis, cirrhosis, and ultimately organ failure that is rapidly becoming a leading cause of liver transplantation. A better understanding of the mechanisms that drive hepatic fibrosis could also reveal improved strategies to treat a variety of important fibrotic diseases including lupus nephritis, cardiovascular fibrosis, radiation induced fibrosis, and idiopathic pulmonary fibrosis.

PUBLICATIONS

1. Type 2 immunity in tissue repair and fibrosis.
   Nat Rev Immunol. 2018 Jan;18(1):62-76.
   Gieseck RL 3rd, Wilson MS, Wynn TA.
   https://www.ncbi.nlm.nih.gov/pubmed/28853443
2. Type 2 immunity is protective in metabolic disease but exacerbates NAFLD collaboratively with TGF-β.
   Sci Transl Med. 2017 Jun 28;9(396).
   Hart KM, Fabre T, Sciurba JC, Gieseck RL 3rd, Borthwick LA, Vannella KM, Acciani TH, de Queiroz Prado R, Thompson RW, White S, Soucy G, Bilodeau M, Ramalingam TR, Arron JR, Shoukry NH, Wynn TA.
   https://www.ncbi.nlm.nih.gov/pubmed/28659437
3. Inflammation and metabolism in tissue repair and regeneration.
   Science. 2017 Jun 9;356(6342):1026-1030.
   Eming SA, Wynn TA, Martin P.
   https://www.ncbi.nlm.nih.gov/pubmed/2859633
4. Interleukin-13 Activates Distinct Cellular Pathways Leading to Ductular Reaction, Steatosis, and Fibrosis.
   Immunity. 2016 Jul 19;45(1):145-58.
   Gieseck RL 3rd, Ramalingam TR, Hart KM, Vannella KM, Cantu DA, Lu WY, Ferreira-González S,
   Forbes SJ, Vallier L, Wynn TA.
   https://www.ncbi.nlm.nih.gov/pubmed/27421703
5. Combinatorial targeting of TSLP, IL-25, and IL-33 in type 2 cytokine-driven inflammation and fibrosis.
   Sci Transl Med. 2016 May 4;8(337):337ra65.
   Vannella KM, Ramalingam TR, Borthwick LA, Barron L, Hart KM, Thompson RW, Kindrachuk KN,
   Cheever AW, White S, Budelsky AL, Comeau MR, Smith DE, Wynn TA.
   https://www.ncbi.nlm.nih.gov/pubmed/27147589

EDUCATION

National Institutes of Health, Postdoctoral Fellow, 1995
University of Wisconsin – Madison, PhD, 1991
Miami University, B.A., 1986

AWARDS & HONORS

Thomson Reuters Highly Cited Researcher. 2014 – 2017
Elected to Fellowship in the American Academy of Microbiology, 2012
National Institutes of Health Merit Award, 2011
Bailey K. Ashford Medal, American Society of Tropical Medicine and Hygiene, 2006
Oswaldo Cruz Medal, Oswaldo Cruz Foundation, 2002

QUOTE

“I joined Pfizer so I could more effectively move basic science discoveries into the clinic so patient lives will be improved”