about
Critical and independent role for SOCS3 in either myeloid or T cells in resistance to Mycobacterium tuberculosisLPS regulates SOCS2 transcription in a type I interferon dependent autocrine-paracrine loop.CD4+ cell-dependent granuloma formation in humanized mice infected with mycobacteria.SOCS3, a Major Regulator of Infection and Inflammation.SOCS3 and STAT3, major controllers of the outcome of infection with Mycobacterium tuberculosis.Downmodulation of Effector Functions in NK Cells upon Toxoplasma gondii Infection.lck-Driven Cre Expression Alters T Cell Development in the Thymus and the Frequencies and Functions of Peripheral T Cell Subsets.Progression of clinical tuberculosis is associated with a Th2 immune response signature in combination with elevated levels of SOCS3.Silencing suppressor of cytokine signaling-1 (SOCS1) in macrophages improves Mycobacterium tuberculosis control in an interferon-gamma (IFN-gamma)-dependent manner.SOCS1 gene expression is increased in severe pulmonary tuberculosis.STAT3 expression by myeloid cells is detrimental for the T- cell-mediated control of infection with Mycobacterium tuberculosis.CISH controls bacterial burden early after infection with Mycobacterium tuberculosis in mice.SOCS2 deletion protects against hepatic steatosis but worsens insulin resistance in high-fat-diet-fed miceSOCS2 expression in bone marrow derived dendritic cells is a positive regulator of T cell activationSpatial and temporal localization of immune transcripts defines hallmarks and diversity in the tuberculosis granuloma
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P50
description
researcher ORCID ID = 0000-0002-8760-6253
@en
wetenschapper
@nl
name
Berit Carow
@ast
Berit Carow
@en
Berit Carow
@es
Berit Carow
@nl
type
label
Berit Carow
@ast
Berit Carow
@en
Berit Carow
@es
Berit Carow
@nl
prefLabel
Berit Carow
@ast
Berit Carow
@en
Berit Carow
@es
Berit Carow
@nl
P31
P496
0000-0002-8760-6253