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Last edited by WorkBot
January 24, 2010 | History

Accessory protein-like is essential for IL-18-mediated signaling 1 edition

Accessory protein-like is essential for IL-18-mediated signaling
Heidi Cheung

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Accessory protein-like is essential for IL-18-mediated signaling.

Published 2005 .
Written in English.

About the Book

Interleukin 18 (IL-18) is an essential cytokine for both innate and adaptive immunity. IL-18 signals through binding to IL-18 receptor alpha (IL-18R), which contains sequence homology to IL-1R and Toll-like receptors (TLRs). While the accessory protein AcP is required for IL-1R signaling, other accessory proteins have roles in regulating TLR signaling. An ACP-like molecule (AcPL) has been identified with the ability to cooperate with IL-18Ralpha in vitro, however, its physiological function remains unknown. Here we demonstrate that IL-18 signals are abolished in AcPL-deficient mice and cells. AcPL-deficient splenocytes fail to respond to IL-18-induced proliferation and interferon-gamma production. AcPL-deficient Th1 cells, dendritic cells and neutrophils also have impaired IL-18-induced activation. Furthermore, AcPL-deficient mice show impaired IL-18-induced NK cytotoxicity. AcPL, however, is dispensable for the activation or inhibition of IL-1R and the various TLR signals that we study. These results suggest that AcPL is a specific cell surface receptor essential for IL-18 signaling.

Edition Notes

Source: Masters Abstracts International, Volume: 44-02, page: 0740.

Thesis (M.Sc.)--University of Toronto, 2005.

Electronic version licensed for access by U. of T. users.

GERSTEIN MICROTEXT copy on microfiche (1 microfiche).

The Physical Object

66 leaves.
Number of pages

ID Numbers

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History Created December 11, 2009 · 2 revisions Download catalog record: RDF / JSON

January 24, 2010 Edited by WorkBot add more information to works
December 11, 2009 Created by WorkBot add works page