Diane Mathis


Division of Immunology, Dept. of Microbiology & Immunobiology
Harvard Medical School
77 Ave. Louis Pasteur
Boston, MA 02115
Tel: 617-432-7742
Fax: 617-432-7744
Email: dm@hms.harvard.edu
Visit my lab page here.






Our lab works in the broad fields of T cell differentiation and tolerance/autoimmunity, translating mechanistic studies on mouse models to normal and diseased humans. Studies on T cell differentiation focus on maturation and selection of the T cell repertoire in the thymus, and on cellular and molecular influences on the “flavor” of T cell responses in the periphery. Studies on autoimmunity explore the immunological mechanisms of type-1 diabetes, rheumatoid arthritis and APECED, in particular central and peripheral mechanisms of T cell tolerance. Major questions tackled are what initiates these diseases, how is their progression regulated, what are the final effector mechanisms, and how do genetic and environmental factors impact disease unfolding. Current foci include: the Aire transcriptional regulatory molecule, Foxp3-expressing Treg cells, immunometabolism and gut microbiota. The application of computational and bioinformatic strategies to these and other issues is one of the lab’s particular strengths. Lastly, we have been engaged in a long-term collaborative effort to develop and apply novel whole-mouse and intravital imaging strategies to immunological problems, especially as concerns mechanisms of autoimmunity.

References:

1. Abramson J, Giraud M, Benoist C and Mathis D. Aire's partners in the molecular control of immunological tolerance. Cell 2010; 140:123-135.

2. Wu HJ, Ivanov II, Darce J, Hattori K, Shima T, Umesaki Y, Littman DR, Benoist C and Mathis D. Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells. Immunity 2010; 32:815-27.

3. Fu W, Wojtkiewicz G, Weissleder R, Benoist C and Mathis D. Early window of diabetes determinism in NOD mice, dependent on the complement receptor CRIg, identified by noninvasive imaging Nature Immunology. 2012; 13:361-368.

4. Cipolletta D, Feuerer M, Li A, Kamei N, Lee J, Shoelson SE, Benoist C and Mathis D. PPAR-gamma is a major driver of the accumulation and phenotype of adipose tissue Treg cells. Nature 2012; 486:549-53.



Last Update: 6/3/2014