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DAVID ARTIS, BSc , PhD
Associate Professor, Department of Pathobiology, University of Pennsylvania, Philadelphia, USA

Director, Penn Gnotobiotic Mouse Facility, University of Pennsylvania

Member, Institute for Immunology, University of Pennsylvania

Member, Immunology Graduate Group Executive Committee, University of Pennsylvania

Member, CAMB/MVP Graduate Group , University of Pennsylvania

Member, Immunology Graduate Group, University of Pennsylvania

Research Areas: Chronic inflammatory diseases, Autoimmune diseases, Parasitic helminth infections, Immunology, Innate immunity, Infectious Disease, Inflammatory diseases, Inflammatory responses, T cells,

Contact Information:
University of Pennsylvania
Perelman School of Medicine
Department of Microbiology
Institute for Immunology
421 Curie Boulevard
BRB II/III, Room 356
 Phone (215) 898-7920
 Email dartis@mail.med.upenn.edu

The goals of the Artis lab are to understand the regulatory mechanisms that control immune cell homeostasis at the body’s barrier surfaces. Employing diverse models of microbial colonization, pathogen infection and chronic inflammation, research in the Artis lab is examining how mammalian host genetics and signals derived from commensal microbial communities influence innate and adaptive immune responses in the skin, lung and intestine.

Studies from a number of labs including the Artis lab, have highlighted that differential colonization of the body’s barrier surfaces by defined commensal bacterial communities can have a profound effect on the development and function of distinct T helper cell populations including Th1, Th2, Th17 and regulatory T cells (Tregs). Dysregulation in the balance of these helper T cell populations can profoundly alter susceptibility to a number of chronic inflammatory diseases including allergy, asthma, arthritis, multiple sclerosis, psoriasis and inflammatory bowel disease. Research in the Artis lab is focusing on how host factors including expression of cytokines and cytokine receptors can influence the balance of helper T cell responses and the development of chronic inflammation.

Recent studies in the Artis lab indicate that innate lymphoid cells, an emerging population of innate cells that express proinflammatory cytokines, may also contribute to the pathogenesis of multiple chronic inflammatory diseases. Innate lymphoid cells are derived from a common Id2-dependent precursor and appear to influence immunity, inflammation and tissue repair and homeostasis in health and disease. Ongoing studies are examining the influence of host- and environmental-derived signals on the development and functions of innate lymphoid cells. The findings of these studies offer the potential to identify new therapeutic targets to limit infection, chronic inflammation and autoimmune diseases.

In addition to host-derived factors, an emerging hypothesis is that alterations in the acquisition and/or composition of beneficial commensal bacteria can profoundly impact helper T cell and innate lymphoid cell responses resulting in susceptibility to multiple infectious and inflammatory diseases. Metagenomic sequencing approaches in patient populations have revealed dysbiosis (alterations of commensal bacterial communities) in patients suffering from multiple inflammatory diseases including arthritis, multiple sclerosis, psoriasis or inflammatory bowel disease. Studies in murine model systems support a causal relationship between alterations in commensal bacteria and chronic inflammation. Studies in the Artis lab are employing germ-free mice and selective antibiotic treatment, coupled with pyrosequencing of bacterial communities, to interrogate the mechanisms through which signals derived from commensal bacteria can influence expression of proinflammatory cytokines and pathogenesis of chronic inflammatory diseases at multiple barrier surfaces.

In a new series of studies, the Artis lab has forged a number of clinical collaborations and began to develop translational research approaches that will allow analysis of findings in murine model systems to be tested in patient populations. Employing tissue samples from clinically-defined patient populations, recent studies are examining the cellular sources of proinflammatory cytokines in the context of allergic diseases, inflammatory bowel disease or psoriasis. These approaches offer the potential to significantly advance our understanding of the pathogenesis of multiple chronic inflammatory diseases.

Alenghat T, Osborne LC, Saenz SA, Kobuley D, Ziegler CG, Mullican SE, Choi I, Grunberg S, Sinha R, Wynosky-Dolfi M, Snyder A., Giacomin PG, Joyce KL, Hoang TB, Bewtra M, Brodsky IE, Sonnenberg GF, Bushman FD, Won K, Lazar MA, Artis D. Histone deacetylase 3 coordinates commensal-bacteria-dependent intestinal homeostasis. Nature : 153-157, 2013.

Siracusa MC, Saenz SA, Tait Wojno ED, Kim BS, Osborne LC, Ziegler C, Benitez AJ, Ruymann KR, Farber DL, Sleiman PM, Hakonarson H, Cianferoni A, Wang ML, Spergel JM, Comeau MR, and Artis D. Thymic stromal lymphopoietin-mediated extramedullary hematopoiesis promotes allergic inflammation. Immunity : 1158-1170, 2013.

Saenz SA, Siracusa MC, Monticelli LA, Ziegler CG, Kim BS, Brestoff JR, Peterson LW, Wherry EJ, Goldrath AW, Bhandoola A, Artis D. IL-25 simultaneously elicits distinct populations of innate lymphoid cells and multipotent progenitor type 2 (MPPtype2) cells. Journal of Experimental Medicine 210: 1823-37, 2013.

Noti M, Tait Wojno ED, Kim BS, Siracusa MC, Giacomin PR, Nair MG, Benitez AJ, Ruymann KR, Muir AB, Hill DA, Chikwava KR, Moghaddam AE, Sattentau QJ, Alex A, Zhou C, Yearley JH, Menard-Katcher P, Kubo M, Obata-Ninomiya K, Karasuyama H, Comeau MR, Brown-Whitehorn T, de Waal Malefyt R, Sleiman PM, Hakonarson H, Cianferoni A, Falk GW, Wang ML, Spergel JM, Artis D. Thymic stromal lymphopoietin-elicited basophil responses promote eosinophilic esophagitis. Nature Medicine 19: 1005-13, 2013.

Qiu J, Guo X, Chen ZM, He L, Sonnenberg GF, Artis D, Fu YX, Zhou L. Group 3 Innate Lymphoid Cells Inhibit T-Cell-Mediated Intestinal Inflammation through Aryl Hydrocarbon Receptor Signaling and Regulation of Microflora. Immunity 39: 386-99, 2013.

Bailis W, Yashiro-Ohtani Y, Fang TC, Hatton RD, Weaver CT, Artis D, Pear WS. Notch simultaneously orchestrates multiple helper T cell programs independently of cytokine signals. Immunity 39: 148-59, 2013.

Hepworth MR, Monticelli LA, Fung TC, Ziegler CG, Grunberg S, Sinha R, Mantegazza AR, Ma HL, Crawford A, Angelosanto JM, Wherry EJ, Koni PA, Bushman FD, Elson CO, Eberl G, Artis D, Sonnenberg GF. Innate lymphoid cells regulate CD4+ T-cell responses to intestinal commensal bacteria. Nature 498: 113-7, 2013.

Roediger B, Kyle R, Yip KH, Sumaria N, Guy TV, Kim BS, Mitchell AJ, Tay SS, Jain R, Forbes-Blom E, Chen X, Tong PL, Bolton HA, Artis D, Paul WE, Fazekas de St Groth B, Grimbaldeston MA, Le Gros G, Weninger W. Cutaneous immunosurveillance and regulation of inflammation by group 2 innate lymphoid cells. Nature Immunology 14: 564-73, 2013.

Tomov VT, Osborne LC, Dolfi DV, Sonnenberg GF, Monticelli LA, Mansfield K, Virgin HW, Artis D, Wherry EJ. Persistent enteric murine norovirus infection is associated with functionally suboptimal virus-specific CD8 T cell responses. Journal of Virology 87: 7015-31, 2013.

Ferreira I, Smyth D, Gaze S, Aziz A, Giacomin P, Ruyssers N, Artis D, Laha T, Navarro S, Loukas A, McSorley HJ. Hookworm excretory/secretory products induce interleukin-4 (IL-4)+ IL-10+ CD4+ T cell responses and suppress pathology in a mouse model of colitis. Infection and Immunity 81: 2104-11, 2013.

BSc (Parasitology (Hons) 1st Class) University of Glasgow, UK, 1995

PhD (Immunology) University of Manchester Medical School, UK, 1998