-
STING knockout mice are as resistant to murine cytomegalovirus infection as wild-type controls, whereas mice with a combined Toll-like receptor/RIG-I-like receptor/STING signaling deficiency do not mount type 1 interferon responses and succumb to the infection.
-
Furthermore, miR-199a suppressed autophagy and interferon-beta (IFN-beta) production by directly targeting TANK-binding kinase 1 (TBK1) mRNA in both J774a.1 and bone marrow-derived macrophage cells.
-
this study shows that IFNbeta inhibits the development of allergen tolerance and is conducive to the development of asthma on subsequent allergen exposure
-
ESAT6 might contribute to virulence of M. tuberculosis by regulating type I IFNs production through TLR4-TRIF signaling pathway.
-
Infection with a helminth parasite attenuates autoimmunity through TGF-beta-mediated suppression of Th17 and Th1 responses.
-
The authors provide evidence that IFIT2 increases the pathological effects of invasive Candida albicans and that administration of interferon-beta has deleterious effects during infection.
-
The expression levels of miR-182, PKR, and IFN-beta are altered in rheumatoid arthritis (RA) and are significantly correlated with the osteoclastogenic capacity of RA monocytes.
-
IFNbeta activates neuronal PI3K/Akt signalling and Akt binds to transcription factor FoxA1 that translocates to the nucleus and induces PDL1. Conversely, inhibition of PI3K/Akt, FoxA1 and PDL1 blocked neuronal ability to generate FoxA1(+)Tregs.
-
Macrophages activated by metabolic endotoxemia infiltrated into islets and produced IFNbeta, which induced beta-cell apoptosis by increasing the expression of Xaf1.
-
Reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) prevented mitochondrial dysfunctions, type I IFN-stimulated transcript levels, inflammatory cell infiltrate, and muscle weakness in an experimental autoimmune myositis mouse model. Thus, these data highlight a central role of mitochondria and ROS in dermatomyositis .
-
Nontypeable Haemophilus influenzae DNA as a Pathogen-Associated Molecular Pattern Molecules triggered I-IFN response, which was STING/TBK1/IRF3 dependent.
-
The Lipopolysaccharide and IFN-beta-mediated increase of STAT1 mRNA and protein levels was abrogated by chelation of Zn(2+) with the membrane permeable chelator N,N,N',N'-Tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) in RAW 264.7 macrophages.
-
MAVS is essential for spontaneous high basal expression of IFN-beta in cardiac myocytes and the heart.
-
Mycobacterium smegmatis induces higher Ifnb expression in macrophages than Mycobacterium avium subspecies.
-
Chronic presence of IFN-I in the brain microenvironment, which negatively affects cognitive function, is mediated via modulation of microglial activity.
-
In experimental autoimmune encephalomyelitis, IFN-beta inhibited downstream inflammatory cytokines through the inhibition of PI3K/AKT/NF-kappaB axis and p38, JNK-MAPK, as well as the regulation of mTOR complexes. Moreover, IFN-beta inhibited Th17 differentiation and influenced the acetylation of the Il17a and Opn gene promoters. IFN-beta plays a role in Th17 differentiation partly through the inhibition of OPN.
-
This review briefly discusses the dysregulation of main T cell subpopulations in CNS autoimmunity and summarized the T cell targeted effects of endogenous and exogenous IFN-beta in health and EAE/MS, with emphasis on the direct actions of IFN-beta on each T cell subset involved in the disease.
-
Rb selectively inhibits innate IFN-beta production by enhancing deacetylation of Ifnb1 promoter, exhibiting a previous unknown non-classical role in innate immunity, which also suggests a role of Rb in the regulation of type I IFN production in inflammatory or autoimmune diseases.
-
c-Cbl negatively regulates IFN-beta signaling and cellular antiviral response by promoting IRF3 ubiquitination and degradation.
-
The effect of topical TREX1 knockdown and local interferon production on HIV transmission in human cervicovaginal explants and humanized mice, is reported.