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Hepatitis B virus hijacks MRE11-RAD50-NBS1 complex to form its minichromosome.
PLoS Pathog
January 2025
State Key Laboratory of Virology and Hubei Province Key Laboratory of Allergy and Immunology, Institute of Medical Virology, TaiKang Medical School, Wuhan University, Wuhan, China.
Chronic hepatitis B virus (HBV) infection can significantly increase the incidence of cirrhosis and liver cancer, and there is no curative treatment. The persistence of HBV covalently closed circular DNA (cccDNA) is the major obstacle of antiviral treatments. cccDNA is formed through repairing viral partially double-stranded relaxed circular DNA (rcDNA) by varies host factors.
View Article and Find Full Text PDFTertiary lymphoid structures in high-grade serous tubo-ovarian carcinoma: anatomical site matters.
Cancer Immunol Immunother
January 2025
Division of Oncology, Department of Clinical Sciences Lund, and Lund University Cancer Center, Lund University, Lund, Sweden.
Tertiary lymphoid structures (TLS) in the tumor microenvironment are prognostically beneficial in many solid cancer types. Reports on TLS in high-grade serous tubo-ovarian carcinoma (HGSC) are few, and the prognostic impact is unclear. We investigated mature TLS (mTLS), immature TLS (iTLS) and lymphoid aggregates (LA) in primary adnexal tumors (PTs) and synchronous omental/peritoneal metastases (pMets) of HGSC.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Northwestern University, Chicago, IL, USA.
Background: Recent advances in Alzheimer's disease (AD) therapeutics involve immunization against amyloid-β (Aβ). Post-mortem brain analysis from the first active Aβ immunotherapy trial indicated clearance of Aβ in some AD patients. Yet, the mechanisms regulating Aβ clearance following immunization remain unknown.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of California, Irvine, Irvine, CA, USA.
Background: Genome-Wide Association Studies (GWAS) identified ApoE4 and Trem2*R47H as two of the strongest genetic risk factors for late-onset Alzheimer's Disease (LOAD). As part of our efforts to develop mouse models that better recapitulate LOAD, at Model Organism Development & Evaluation for Late-Onset Alzheimer's Disease (MODEL-AD) consortium at University of California - Irvine, we have created a triple homozygous mouse model that combines our previously developed hAb-KI mice (Jackson Lab #031050), Trem2 (Jackson Lab #034036) and a humanized ApoE4 (Jackson Lab #027894), to evaluate the interactions between aging, hAPOE4, TREM2*R47H, and hAb.
Method: By breeding the hAb-KI, hApoE4 and Trem2, we obtained triple homozygous (HO) mice and we then generated four different groups: WT (C57BL6/J), hAb-KI HO, hAb-KI HO;hApoE4 HO and hAb-KI HO;hApoE4 HO;Trem2 HO.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Knight Alzheimer Disease Research Center, St. Louis, MO, USA.
Background: Alzheimer's disease (AD) is characterized by the aggregation and accumulation of proteins including amyloid-β and tau. We previously compared the immunological milieus in the brain of mice with amyloid deposition or tau aggregation and found that mice with tauopathy but not amyloid developed a unique adaptive immune response with markedly increased activated T cells in areas with tau pathology. T cell depletion blocked tau-mediated neurodegeneration.
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