Lineage specific role of Ship1 in development of allergic airway inflammation

Matthew J Gold; Michael R Hughes; Frann Antignano; Colby Zaph; Kelly M McNagny

doi:10.1186/1710-1492-10-S2-A56

Lineage specific role of Ship1 in development of allergic airway inflammation

Matthew J Gold, Michael R Hughes, Frann Antignano, Colby Zaph, Kelly M McNagny

Research output: Contribution to conference › Abstract

Abstract

The PI3K pathway is a potent mediator of several functions associated with asthma pathogenesis, including supporting leukocyte survival, activation, migration andcytokine release. Proper negative regulation of this pathway is integral in order to restrict overactive immune responses. Negative regulation of PI3K is predominantly controlled by the lipid phosphatases PTEN and SHIP-1. Inpp5d (Ship1) deficient mice develop spontaneous airway inflammation and have enhanced sensitivity to allergen induced airway inflammation. We hypothesized that deleting Ship1 expression specifically in lineages known to be crucial for adaptive Th2 responses would uncover more subtle effects that could either positively or negatively regulate disease severity in a mouse model of allergic airway inflammation (AAI).

Original language	English
Number of pages	1
DOIs	https://doi.org/10.1186/1710-1492-10-S2-A56
Publication status	Published - 18 Dec 2014
Externally published	Yes
Event	Canadian Society of Allergy and Clinical Immunology : Annual Scientific Meeting 2014 - Ottawa, ON, Canada Duration: 23 Oct 2014 → 26 Oct 2014

Other

Other	Canadian Society of Allergy and Clinical Immunology
Country/Territory	Canada
City	Ottawa, ON
Period	23/10/14 → 26/10/14

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10.1186/1710-1492-10-S2-A56

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title = "Lineage specific role of Ship1 in development of allergic airway inflammation",

abstract = "The PI3K pathway is a potent mediator of several functions associated with asthma pathogenesis, including supporting leukocyte survival, activation, migration andcytokine release. Proper negative regulation of this pathway is integral in order to restrict overactive immune responses. Negative regulation of PI3K is predominantly controlled by the lipid phosphatases PTEN and SHIP-1. Inpp5d (Ship1) deficient mice develop spontaneous airway inflammation and have enhanced sensitivity to allergen induced airway inflammation. We hypothesized that deleting Ship1 expression specifically in lineages known to be crucial for adaptive Th2 responses would uncover more subtle effects that could either positively or negatively regulate disease severity in a mouse model of allergic airway inflammation (AAI).",

author = "Gold, \{Matthew J\} and Hughes, \{Michael R\} and Frann Antignano and Colby Zaph and McNagny, \{Kelly M\}",

year = "2014",

month = dec,

day = "18",

doi = "10.1186/1710-1492-10-S2-A56",

language = "English",

note = "Canadian Society of Allergy and Clinical Immunology : Annual Scientific Meeting 2014 ; Conference date: 23-10-2014 Through 26-10-2014",

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TY - CONF

T1 - Lineage specific role of Ship1 in development of allergic airway inflammation

AU - Gold, Matthew J

AU - Hughes, Michael R

AU - Antignano, Frann

AU - Zaph, Colby

AU - McNagny, Kelly M

PY - 2014/12/18

Y1 - 2014/12/18

N2 - The PI3K pathway is a potent mediator of several functions associated with asthma pathogenesis, including supporting leukocyte survival, activation, migration andcytokine release. Proper negative regulation of this pathway is integral in order to restrict overactive immune responses. Negative regulation of PI3K is predominantly controlled by the lipid phosphatases PTEN and SHIP-1. Inpp5d (Ship1) deficient mice develop spontaneous airway inflammation and have enhanced sensitivity to allergen induced airway inflammation. We hypothesized that deleting Ship1 expression specifically in lineages known to be crucial for adaptive Th2 responses would uncover more subtle effects that could either positively or negatively regulate disease severity in a mouse model of allergic airway inflammation (AAI).

AB - The PI3K pathway is a potent mediator of several functions associated with asthma pathogenesis, including supporting leukocyte survival, activation, migration andcytokine release. Proper negative regulation of this pathway is integral in order to restrict overactive immune responses. Negative regulation of PI3K is predominantly controlled by the lipid phosphatases PTEN and SHIP-1. Inpp5d (Ship1) deficient mice develop spontaneous airway inflammation and have enhanced sensitivity to allergen induced airway inflammation. We hypothesized that deleting Ship1 expression specifically in lineages known to be crucial for adaptive Th2 responses would uncover more subtle effects that could either positively or negatively regulate disease severity in a mouse model of allergic airway inflammation (AAI).

UR - https://www.scopus.com/pages/publications/84961664711

U2 - 10.1186/1710-1492-10-S2-A56

DO - 10.1186/1710-1492-10-S2-A56

M3 - Abstract

AN - SCOPUS:84961664711

T2 - Canadian Society of Allergy and Clinical Immunology

Y2 - 23 October 2014 through 26 October 2014

ER -

Lineage specific role of Ship1 in development of allergic airway inflammation

Abstract

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