Response to comment on "activation of β-catenin in dendritic cells regulates immunity versus tolerance in the intestine"

Santhakumar Manicassamy; Bali Pulendran

doi:10.1126/science.1198771

Response to comment on "activation of β-catenin in dendritic cells regulates immunity versus tolerance in the intestine"

Santhakumar Manicassamy, Bali Pulendran

Research output: Contribution to journal › Comment/debate › peer-review

1 Scopus citations

Abstract

Murphy argues that deletion of β-catenin in macrophages is a caveat to our interpretation that Wnt signaling programs dendritic cells (DCs) into a tolerogenic state in the gut. However, our data demonstrate that β-catenin-deficient DCs are greatly impaired in inducing regulatory T cells, and induce enhanced T helper 17 (T _H17)/T _H1 responses. Assessing the relative importance of DCs versus macrophages in intestinal tolerance must await tools that permit the genetic deletion of the numerous DC and macrophage subsets in the intestine.

Original language	English (US)
Pages (from-to)	405b
Journal	Science
Volume	333
Issue number	6041
DOIs	https://doi.org/10.1126/science.1198771
State	Published - Jul 22 2011
Externally published	Yes

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abstract = "Murphy argues that deletion of β-catenin in macrophages is a caveat to our interpretation that Wnt signaling programs dendritic cells (DCs) into a tolerogenic state in the gut. However, our data demonstrate that β-catenin-deficient DCs are greatly impaired in inducing regulatory T cells, and induce enhanced T helper 17 (T H17)/T H1 responses. Assessing the relative importance of DCs versus macrophages in intestinal tolerance must await tools that permit the genetic deletion of the numerous DC and macrophage subsets in the intestine.",

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AU - Pulendran, Bali

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N2 - Murphy argues that deletion of β-catenin in macrophages is a caveat to our interpretation that Wnt signaling programs dendritic cells (DCs) into a tolerogenic state in the gut. However, our data demonstrate that β-catenin-deficient DCs are greatly impaired in inducing regulatory T cells, and induce enhanced T helper 17 (T H17)/T H1 responses. Assessing the relative importance of DCs versus macrophages in intestinal tolerance must await tools that permit the genetic deletion of the numerous DC and macrophage subsets in the intestine.

AB - Murphy argues that deletion of β-catenin in macrophages is a caveat to our interpretation that Wnt signaling programs dendritic cells (DCs) into a tolerogenic state in the gut. However, our data demonstrate that β-catenin-deficient DCs are greatly impaired in inducing regulatory T cells, and induce enhanced T helper 17 (T H17)/T H1 responses. Assessing the relative importance of DCs versus macrophages in intestinal tolerance must await tools that permit the genetic deletion of the numerous DC and macrophage subsets in the intestine.

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ER -

Response to comment on "activation of β-catenin in dendritic cells regulates immunity versus tolerance in the intestine"

Abstract

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