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Peptide-Drug Conjugate for Therapeutic Reprogramming of Tumor-Associated Macrophages in Breast Cancer.
Adv Sci (Weinh)
January 2025
Institute of Biomedicine and Translational Medicine, University of Tartu, Ravila 14B, Tartu, 50411, Estonia.
In triple-negative breast cancer (TNBC), pro-tumoral macrophages promote metastasis and suppress the immune response. To target these cells, a previously identified CD206 (mannose receptor)-binding peptide, mUNO was engineered to enhance its affinity and proteolytic stability. The new rationally designed peptide, MACTIDE, includes a trypsin inhibitor loop, from the Sunflower Trypsin Inhibitor-I.
View Article and Find Full Text PDFAssessment of heat-killed expressing Chikungunya virus E2 protein as a candidate vaccine for dual protection against Chikungunya virus and .
Front Immunol
January 2025
Nanobioscience Group, Agharkar Research Institute, Pune, India.
The Chikungunya virus (CHIKV) is a mosquito-borne virus with a long history of recurring epidemics transmitted through mosquitoes. The rapid spread of CHIKV has intensified the need for potent vaccines. Escherichia coli (), a vital part of human gut microbiota, is utilized in recombinant DNA technology for cloning.
View Article and Find Full Text PDFC-X-C chemokine receptor type 5CD8 T cells as immune regulators in hepatitis Be antigen-positive chronic hepatitis B under interferon-alpha treatment.
World J Gastroenterol
January 2025
Institute of Hepatology and Department of Infectious Diseases, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, China.
Background: C-X-C chemokine receptor type 5 (CXCR5)CD8 T cells represent a unique immune subset with dual roles, functioning as cytotoxic cells in persistent viral infections while promoting B cell responses. Despite their importance, the specific role of CXCR5CD8 T cells in chronic hepatitis B (CHB), particularly during interferon-alpha (IFN-α) treatment, is not fully understood. This study aims to elucidate the relationship between CXCR5CD8 T cells and sustained serologic response (SR) in patients undergoing 48 weeks of pegylated IFN-α (peg-IFN-α) treatment for CHB.
View Article and Find Full Text PDFOpportunities for predictive proteogenomic biomarkers of drug treatment sensitivity in epithelial ovarian cancer.
Front Oncol
January 2025
Department of Laboratory Medicine and Pathology, University of Minnesota School of Medicine, Minneapolis, MN, United States.
Genomic analysis has played a significant role in the identification of driver mutations that are linked to disease progression and response to drug treatment in ovarian cancer. A prominent example is the stratification of epithelial ovarian cancer (EOC) patients with homologous recombination deficiency (HRD) characterized by mutations in DNA damage repair genes such as for treatment with PARP inhibitors. However, recent studies have shown that some epithelial ovarian tumors respond to PARP inhibitors irrespective of their HRD or mutation status.
View Article and Find Full Text PDFImpact of endoplasmic reticulum aminopeptidases 1 (ERAP1) and 2 (ERAP2) on neutrophil cellular functions.
Front Cell Dev Biol
January 2025
Dipartimento di Scienze Biomediche e Cliniche, Università degli Studi di Milano, Milano, Italy.
Introduction: Endoplasmic reticulum aminopeptidases 1 (ERAP1) and 2 (ERAP2) modulate a plethora of physiological processes for the maintenance of homeostasis in different cellular subsets at both intra and extracellular level.
Materials And Methods: In this frame, the extracellular supplementation of recombinant human (rh) ERAP1 and ERAP2 (300 ng/ml) was used to mimic the effect of stressor-induced secretion of ERAPs on neutrophils isolated from 5 healthy subjects. In these cells following 3 h or 24 h rhERAP stimulation by Western Blot, RT-qPCR, Elisa, Confocal microscopy, transwell migration assay, Oxygraphy and Flow Cytometry we assessed: i) rhERAP internalization; ii) activation; iii) migration; iv) oxygen consumption rate; v) reactive oxygen species (ROS) accumulation; granule release; vi) phagocytosis; and vii) autophagy.
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