Halotis Pourtales
Veronica CanelaStamp of Ifni
Zoomers of the Sunshine Coast 🇨🇦Type I interferon signalling, cognition and neurodegeneration following COVID-19: update on a mechanistic pathogenetic model with implications for Alzheimer’s disease.
Selective vulnerability of neurogenesis sites to IFN-I dysregulation would then lead to clinical manifestations such as anosmia and cognitive impairment.
#Neurodegeneration #CognitiveDysfunction #IFNI
https://www.frontiersin.org/articles/10.3389/fnhum.2024.1352118/full
Type I interferon signaling, cognition and neurodegeneration following COVID-19: update on a mechanistic pathogenetic model with implications for Alzheimer’s disease
COVID-19’s effects on the human brain reveal a multifactorial impact on cognition and the potential to inflict lasting neuronal damage. Type I interferon signaling, a pathway that represents our defense against pathogens, is primarily affected by COVID-19. Type I interferon signaling, however, is known to mediate cognitive dysfunction upon its dysregulation following synaptopathy, microgliosis and neuronal damage. In previous studies, we proposed a model of outside-in dysregulation of tonic IFN-I signaling in the brain following a COVID-19. This disruption would be mediated by the crosstalk between central and peripheral immunity, and could potentially establish feed-forward IFN-I dysregulation leading to neuroinflammation and potentially, neurodegeneration. We proposed that for the CNS, the second-order mediators would be intrinsic disease-associated molecular patterns (DAMPs) such as proteopathic seeds, without the requirement of neuroinvasion to sustain inflammation. Selective vulnerability of neurogenesis sites to IFN-I dysregulation would then lead to clinical manifestations such as anosmia and cognitive impairment. Since the inception of our model at the beginning of the pandemic, a growing body of studies has provided further evidence for the effects of SARS-CoV-2 infection on the human CNS and cognition. Several preclinical and clinical studies have displayed IFN-I dysregulation and tauopathy in gene expression and neuropathological data in new cases, corresponding...
Judit Svensson ArvelundCool paper dissecting the mechanism of action of #immunecheckpointblockade, anti-CTLA-4, and showing the important role of #myeloidcells #macrophages
"Anti-CTLA-4 antibodies drive myeloid activation and reprogram the tumor microenvironment through FcγR engagement and type I interferon signaling"
#naturecancer #immunotherapy #immunecheckpointinhibitor #macrophages #IFNI
Anti-CTLA-4 antibodies drive myeloid activation and reprogram the tumor microenvironment through FcγR engagement and type I interferon signaling - Nature Cancer
Yofe et al. demonstrate that FcγR engagement early after anti-CTLA-4 blockade induces a rapid remodeling of innate immunity and activation of type I interferon signaling, which are crucial for successful anti-CTLA-4 therapy.