Tick Salivary Sialostatin L Represses the Initiation of/nImmune Responses by Targeting IRF4-Dependent/nTranscription in Murine Mast Cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60077344%3A_____%2F15%3A00453380" target="_blank" >RIV/60077344:_____/15:00453380 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.4049/jimmunol.1401823" target="_blank" >http://dx.doi.org/10.4049/jimmunol.1401823</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.4049/jimmunol.1401823" target="_blank" >10.4049/jimmunol.1401823</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Tick Salivary Sialostatin L Represses the Initiation of/nImmune Responses by Targeting IRF4-Dependent/nTranscription in Murine Mast Cells

Popis výsledku v původním jazyce

Coevolution of ticks and the vertebrate immune system has led to the development of immunosuppressive molecules that prevent immediate response of skin-resident immune cells to quickly fend off the parasite. In this article, we demonstrate that the tick-derived immunosuppressor sialostatin L restrains IL-9 production by mast cells, whereas degranulation and IL-6 expression are both unaffected. In addition, the expression of IL-1 beta and IRF4 is strongly reduced in the presence of sialostatin L. Correspondingly, IRF4-or IL-1R-deficient mast cells exhibit a strong impairment in IL-9 production, demonstrating the importance of IRF4 and IL-1 in the regulation of the Il9 locus in mast cells. Furthermore, IRF4 binds to the promoters of Il1b and Il9, suggesting that sialostatin L suppresses mast cell-derived IL-9 preferentially by inhibiting IRF4. In an experimental asthma model, mast cell-specific deficiency in IRF4 or administration of sialostatin L results in a strong reduction in asthma

Název v anglickém jazyce

Tick Salivary Sialostatin L Represses the Initiation of/nImmune Responses by Targeting IRF4-Dependent/nTranscription in Murine Mast Cells

Popis výsledku anglicky

Coevolution of ticks and the vertebrate immune system has led to the development of immunosuppressive molecules that prevent immediate response of skin-resident immune cells to quickly fend off the parasite. In this article, we demonstrate that the tick-derived immunosuppressor sialostatin L restrains IL-9 production by mast cells, whereas degranulation and IL-6 expression are both unaffected. In addition, the expression of IL-1 beta and IRF4 is strongly reduced in the presence of sialostatin L. Correspondingly, IRF4-or IL-1R-deficient mast cells exhibit a strong impairment in IL-9 production, demonstrating the importance of IRF4 and IL-1 in the regulation of the Il9 locus in mast cells. Furthermore, IRF4 binds to the promoters of Il1b and Il9, suggesting that sialostatin L suppresses mast cell-derived IL-9 preferentially by inhibiting IRF4. In an experimental asthma model, mast cell-specific deficiency in IRF4 or administration of sialostatin L results in a strong reduction in asthma

Druh

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

CEP obor

EC - Imunologie

OECD FORD obor

—

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2015

Kód důvěrnosti údajů

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

Název periodika

Journal of Immunology

ISSN

0022-1767

e-ISSN

—

Svazek periodika

195

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

621-631

Kód UT WoS článku

000358066800022

EID výsledku v databázi Scopus

—