Shb deficient mice display an augmented TH2 response in peripheral CD4+ T cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F11%3A00051960" target="_blank" >RIV/00216224:14310/11:00051960 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68081707:_____/11:00440859

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Shb deficient mice display an augmented TH2 response in peripheral CD4+ T cells

Popis výsledku v původním jazyce

BACKGROUND: Shb, a ubiquitously expressed Src homology 2 domain-containing adaptor protein has previously been implicated in the signaling of various tyrosine kinase receptors including the TCR. Shb associates with SLP76, LAT and Vav, all important components in the signaling cascade governing T cell function and development. A Shb knockout mouse was recently generated and the aim of the current study was to address the importance of Shb deficiency on T cell development and function. RESULTS: Shb knockout mice did not display any major changes in thymocyte development despite an aberrant TCR signaling pattern, including increased basal activation and reduced stimulation-induced phosphorylation. The loss of Shb expression did however affect peripheral CD4+ T(H) cells resulting in an increased proliferative response to TCR stimulation and an elevated IL-4 production of naive T(H) cells. This suggests a T(H)2 skewing of the Shb knockout immune system, seemingly caused by an altered TCR si

Název v anglickém jazyce

Shb deficient mice display an augmented TH2 response in peripheral CD4+ T cells

Popis výsledku anglicky

BACKGROUND: Shb, a ubiquitously expressed Src homology 2 domain-containing adaptor protein has previously been implicated in the signaling of various tyrosine kinase receptors including the TCR. Shb associates with SLP76, LAT and Vav, all important components in the signaling cascade governing T cell function and development. A Shb knockout mouse was recently generated and the aim of the current study was to address the importance of Shb deficiency on T cell development and function. RESULTS: Shb knockout mice did not display any major changes in thymocyte development despite an aberrant TCR signaling pattern, including increased basal activation and reduced stimulation-induced phosphorylation. The loss of Shb expression did however affect peripheral CD4+ T(H) cells resulting in an increased proliferative response to TCR stimulation and an elevated IL-4 production of naive T(H) cells. This suggests a T(H)2 skewing of the Shb knockout immune system, seemingly caused by an altered TCR si

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FN - Epidemiologie, infekční nemoci a klinická imunologie

OECD FORD obor

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Projekt

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Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2011

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

BMC immunology

ISSN

1471-2172

e-ISSN

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Svazek periodika

12

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

SE - Švédské království

Počet stran výsledku

10

Strana od-do

1-10

Kód UT WoS článku

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EID výsledku v databázi Scopus

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