Notch signaling is an important regulator of type 2 immunity

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 mi...

Full description

Saved in:
Bibliographic Details
Published inThe Journal of experimental medicine Vol. 202; no. 8; pp. 1037 - 1042
Main Authors Tu, Lili, Fang, Terry C, Artis, David, Shestova, Olga, Pross, Seth E, Maillard, Ivan, Pear, Warren S
Format Journal Article
LanguageEnglish
Published United States The Rockefeller University Press 17.10.2005
Subjects
Animals
Blotting, Southern
Brief Definitive Report
CD4-Positive T-Lymphocytes - immunology
Cell Differentiation - immunology
DNA Primers
Flow Cytometry
Green Fluorescent Proteins
Immunity, Cellular - immunology
Leishmania - immunology
Leishmania major
Mice
Mice, Transgenic
Receptors, Notch - metabolism
Signal Transduction - immunology
Th2 Cells - metabolism
Trichuris - immunology
Trichuris muris
Online AccessGet full text

Cover

More Information
Summary: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.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
L. Tu, T.C. Fang, and D. Artis contributed equally to this work.
CORRESPONDENCE Warren S. Pear: wpear@mail.med.upenn.edu
ISSN:0022-1007
1540-9538
1892-1007
DOI:10.1084/jem.20050923