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Cited by 284

The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.

Notch signaling is an important regulator of type 2 immunity

Open access
Tu, LiLi, Fang, Terry C., Artis, David, Shestova, Olga, Pross, Seth E., Maillard, Ivan, Pear, Warren S.·2005·The Journal of Experimental Medicine

Abstract

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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Crossref · 10.1084/jem.20050923

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Metadata

Authors
Tu, L., Fang, T. C., Artis, D., Shestova, O., Pross, S. E., Maillard, I., & Pear, W. S.
Venue
The Journal of Experimental Medicine
Published
2005-10-17
Volume
202
Issue
8
Pages
1037-1042
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2145499731
Cited by
284
References
28
FWCI
6.44
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Notch signaling is an important regulator of type 2 immunity. https://app.cochat.ai/papers/10.1084/jem.20050923
The paper
Tu, L., Fang, T. C., Artis, D., Shestova, O., Pross, S. E., Maillard, I., & Pear, W. S. (2005). Notch signaling is an important regulator of type 2 immunity. The Journal of Experimental Medicine. https://doi.org/10.1084/jem.20050923

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.