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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Laboratory of Behavioral Neuroscience, National Institute on Aging, Intramural Research Program, Baltimore, MD, USA.
Background: While immune function is known to play a mechanistic role in Alzheimer's disease (AD), whether immune proteins in peripheral circulation influence the rate of amyloid-b (Aβ) progression remains unknown.
Method: Using the Baltimore Longitudinal Study of Aging (BLSA; n = 196; mean follow-up: 5 years/4 scans), we identified immune-related proteins in plasma (candidate proteins) related to rates of change in cortical Aβ levels, as measured by C-PiB PET. Along with identifying genetic variants that contributed to candidate protein associations, characterizing their relationships with tau-PET and changes in ADRD biomarkers (Aβ, NfL, GFAP, pTau-181), and assessing their expression patterns in human microglia, we leveraged data from the Atherosclerosis Risk in Communities (ARIC) study to determine if changes in candidate protein levels precede Ab = β onset (n = 272), and whether they predict 20-year dementia risk during mid-life (n = 11,596) and 8-year dementia risk during late-life (n = 4,288).
Evaluation of the immunogenicity of a DNA vaccine for Leishmania major based on the Leishmania-activated C kinase antigen using calcium phosphate and chitosan adjuvants.
Trans R Soc Trop Med Hyg
January 2025
Department of Medical Parasitology, Medical school, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 6135715794, Iran.
Background: Leishmaniasis represents a significant parasitic disease with global health implications, and the development of an affordable and effective vaccine could provide a valuable solution. This study aimed to evaluate the immunogenicity of a DNA vaccine targeting Leishmania major specifically based on the Leishmania-activated C kinase (LACK) antigen, utilizing calcium phosphate nanoparticles (CaPNs) and chitosan nanoparticles (ChitNs) as adjuvants.
Methods: Seventy female BALB/c mice, aged 4-6 wk and weighing 20-22 g, were selected and divided into five groups, each consisting of 14 mice.
HDAC6 deacetylates TRIM56 to negatively regulate cGAS-STING-mediated type I interferon responses.
EMBO Rep
January 2025
Institute of Biomedicine, College of Life Science and Technology, Guangdong Province Key Laboratory of Bioengineering Medicine, Key Laboratory of Innovative Technology Research on Natural Products and Cosmetics Raw Materials, Jinan University, 510632, Guangzhou, China.
Histone deacetylase HDAC6 has been implicated in regulating antiviral innate immunity. However, its precise function in response to DNA virus infection remains elusive. Herein, we find that HDAC6 deficiency promotes the activation of cGAS-STING signaling and type I interferon (IFN) production, both in vitro and in vivo, resulting in a decrease in HSV-1 infection.
View Article and Find Full Text PDFRemodelling of the immune landscape by IFNγ counteracts IFNγ-dependent tumour escape in mouse tumour models.
Nat Commun
January 2025
The Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
Loss of IFNγ-sensitivity by tumours is thought to be a mechanism enabling evasion, but recent studies suggest that IFNγ-resistant tumours can be sensitised for immunotherapy, yet the underlying mechanism remains unclear. Here, we show that IFNγ receptor-deficient B16-F10 mouse melanoma tumours are controlled as efficiently as WT tumours despite their lower MHC class I expression. Mechanistically, IFNγ receptor deletion in B16-F10 tumours increases IFNγ availability, triggering a remodelling of the immune landscape characterised by inflammatory monocyte infiltration and the generation of 'mono-macs'.
View Article and Find Full Text PDFImmunometabolic shifts in autoimmune disease: Mechanisms and pathophysiological implications.
Autoimmun Rev
December 2024
Department of Rheumatology and Immunology, Changzheng Hospital, Naval Medical University, Shanghai, China. Electronic address:
Autoimmune diseases occur when the immune system abnormally attacks the body's normal tissues, causing inflammation and damage. Each disease has unique immune and metabolic dysfunctions during pathogenesis. In rheumatoid arthritis (RA), immune cells have different metabolic patterns and mitochondrial/lysosomal dysfunctions at different disease stages.
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