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A critical role for SOCS3 in innate resistance to Toxoplasma gondii.

Abstract：

:The innate and adaptive immune responses that confer resistance to the intracellular pathogen Toxoplasma gondii critically depend on IL-12 production, which drives interferon-γ (IFN-γ) expression. Certain cytokines can activate STAT3 and limit IL-12 production to prevent infection-associated immune pathology, but T. gondii also directly activates STAT3 to evade host immunity. We show that suppressor of cytokine signaling molecule 3 (SOCS3), a target of STAT3 that limits signaling by the pleiotropic cytokine IL-6, is upregulated in response to infection but is dispensable for the immune-inhibitory effects of T. gondii. Unexpectedly, mice with targeted deletion of SOCS3 in macrophages and neutrophils have reduced IL-12 responses and succumb to toxoplasmosis. Anti-IL-6 administration or IL-12 treatment blocked disease susceptibility, suggesting that in the absence of SOCS3, macrophages are hypersensitive to the anti-inflammatory properties of IL-6. Thus, SOCS3 has a critical role in suppressing IL-6 signals and promoting immune responses to control T. gondii infection.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Whitmarsh RJ,Gray CM,Gregg B,Christian DA,May MJ,Murray PJ,Hunter CA

doi

10.1016/j.chom.2011.07.009

subject

Has Abstract

pub_date

2011-09-15 00:00:00

pages

224-36

issue

3

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(11)00230-7

journal_volume

10

pub_type

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