Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 202, Issue 8, Pages 1037-1042Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20050923
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Funding
- NHLBI NIH HHS [T32 HL007439, T32HL007439-27] Funding Source: Medline
- NIAID NIH HHS [R01 AI061570, AI61570] Funding Source: Medline
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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.
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