The Journal of Experimental Medicine
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Published 17 October 2005. doi:10.1084/jem.20050923
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 8, 1037-1042
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BRIEF DEFINITIVE REPORT

Notch signaling is an important regulator of type 2 immunity

LiLi Tu1,2,3, Terry C. Fang1,2,3, David Artis4, Olga Shestova1,2,3, Seth E. Pross1,2,3, Ivan Maillard2,5, and Warren S. Pear1,2,3

1 Department of Pathology and Laboratory Medicine, School of Veterinary Medicine
2 Abramson Family Cancer Research Institute, School of Veterinary Medicine
3 Institute for Medicine and Engineering, School of Veterinary Medicine
4 Department of Pathobiology, School of Veterinary Medicine
5 Division of Hematology-Oncology, University of Pennsylvania, Philadelphia, PA 19104

CORRESPONDENCE Warren S. Pear: wpear{at}mail.med.upenn.edu

Notch ligands and receptors have been implicated in helper T cell (Th cell) differentiation. Whether Notch signals are involved in differentiation of T helper type 1 (Th1) cells, Th2 cells, or both, however, remains unresolved. To clarify the role of Notch in Th cell differentiation, we generated mice that conditionally inactivate Notch signaling in mature T cells. Mice that lack Notch signaling in CD4+ T cells fail to develop a protective Th2 cell response against the gastrointestinal helminth Trichuris muris. In contrast, they exhibit effective Th1 cell responses and are able to control Leishmania major infection. These data demonstrate that Notch signaling is a regulator of type 2 immunity.


L. Tu, T.C. Fang, and D. Artis contributed equally to this work.


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