BBS Faculty Member - Ramnik Xavier

Ramnik Xavier

Center for Computational and Integrative Biology

Massachusetts General Hospital
Center for Computational & Integrative Biology
185 Cambridge Street - Simches 7222
Boston, MA 02114
Tel: 617-643-3331
Fax: 617-643-3328

Institute Member
Broad Institute of Harvard and MIT
415 Main St., 7th Floor
Cambridge, MA 02142
Visit my lab page here.

The primary research goal of the Xavier Laboratory at Massachusetts General Hospital and the Broad Institute is to discover and understand the function of important mediators and effectors involved in both the innate and adaptive immune systems. Of particular interest are the cellular components and regulatory networks that interact dynamically within temporal, spatial, and patho-physiological contexts of innate immunity. A second area of focus is to examine the pathway defects associated with genetic variants in inflammatory bowel disease and identify novel small molecules that interrupt signal transduction pathways associated with disease risk. We are pursuing integrative systems approaches that closely couple genome-wide experimentation with high-throughput assays and computational methods. Furthermore, we are pursuing studies of the microbiome in autoimmunity and inflammatory bowel disease.

Crohn’s disease and ulcerative colitis are debilitating inflammatory diseases of the gastrointestinal tract collectively known as inflammatory bowel diseases (IBD). Among complex diseases, genetics has been particularly successful in the identification of genes for IBD, with recent efforts in genome-wide association studies bringing the total number of loci to more than 160. These studies have highlighted the significance of the relationship between intracellular responses to microbes and the regulation of adaptive immunity in the pathogenesis of IBD. With rapid progress in human genetics, it has become clear that a major challenge in the study of complex genetic traits is to determine how disease genes and their corresponding alleles exert their influence on the biology of health and disease. The lab focuses on applying novel genomic, genetic, and chemical biology approaches to gain insights into the function of genetic variants underlying common inflammatory disease and to explore the potential for reversing the effects of susceptibility alleles. We are also investigating relationships between IBD and the gut microbiome, including interactions between host genetics and gut microbiota.

Last Update: 8/11/2015


For a complete listing of publications click here.



Begun J, Lassen KG, Jijon HB, Baxt LA, Goel G, Heath RJ, Ng A, Tam JM, Kuo SY, Villablanca EJ, Fagbami L, Oosting M, Kumar V, Schenone M, Carr SA, Joosten LA, Vyas JM, Daly MJ, Netea MG, Brown GD, Wijmenga C, Xavier RJ. Integrated Genomics of Crohn's Disease Risk Variant Identifies a Role for CLEC12A in Antibacterial Autophagy. Cell Rep. 2015;11(12):1905-18. PMID: 26095365.

Kostic AD, Gevers D, Siljander H, Vatanen T, Hyotylainen T, Hamalainen AM, Peet A, Tillmann V, Poho P, Mattila I, Lahdesmaki H, Franzosa EA, Vaarala O, de Goffau M, Harmsen H, Ilonen J, Virtanen SM, Clish CB, Oresic M, Huttenhower C, Knip M, Group DS, Xavier RJ. The dynamics of the human infant gut microbiome in development and in progression toward type 1 diabetes.
Cell Host Microbe. 2015;17(2):260-73. PMID: 25662751.

Khor B, Gagnon JD, Goel G, Roche MI, Conway KL, Tran K, Aldrich LN, Sundberg TB, Paterson AM, Mordecai S, Dombkowski D, Schirmer M, Tan PH, Bhan AK, Roychoudhuri R, Restifo NP, O'Shea JJ, Medoff BD, Shamji AF, Schreiber SL, Sharpe AH, Shaw SY, Xavier RJ. The kinase DYRK1A reciprocally regulates the differentiation of Th17 and regulatory T cells.
Elife. 2015;4. PMID: 25998054.

Graham DB, Becker CE, Doan A, Goel G, Villablanca EJ, Knights D, Mok A, Ng AC, Doench JG, Root DE, Clish CB, Xavier RJ. Functional genomics identifies negative regulatory nodes controlling phagocyte oxidative burst.
Nat Commun. 2015;6:7838. PMID: 26194095.

Lassen KG, Kuballa P, Conway KL, Patel KK, Becker CE, Peloquin JM, Villablanca EJ, Norman JM, Liu TC, Heath RJ, Becker ML, Fagbami L, Horn H, Mercer J, Yilmaz OH, Jaffe JD, Shamji AF, Bhan AK, Carr SA, Daly MJ, Virgin HW, Schreiber SL, Stappenbeck TS, Xavier RJ. Atg16L1 T300A variant decreases selective autophagy resulting in altered cytokine signaling and decreased antibacterial defense.
Proc Natl Acad Sci U S A. 2014;111(21):7741-6. PMID: 24821797.

© 2015 by the President and Fellows of Harvard College