Parasitic diseases have worldwide medical and economical impact. Host T lymphocytes and the cytokines they produce determine the outcome of parasitic infections. Programmed cell death by apoptosis is induced in the course of parasitic infections, and affects cytokine production by removing activated effector T and B cells. In addition, engulfment of apoptotic cells promotes the secretion of cytokines that regulate intracellular replication of protozoan parasites. In this review, we discuss how the cross-talk between apoptosis and cytokines regulates parasitic infection.
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http://dx.doi.org/10.1016/j.cytogfr.2007.01.009 | DOI Listing |
Clin Transl Med
December 2024
Andalusian Center of Molecular Biology and Regenerative Medicine-CABIMER, Junta de Andalucía-University of Pablo de Olavide-University of Seville-CSIC, Seville, Spain.
Background: The complex aetiology of type 1 diabetes (T1D), characterised by a detrimental cross-talk between the immune system and insulin-producing beta cells, has hindered the development of effective disease-modifying therapies. The discovery that the pharmacological activation of LRH-1/NR5A2 can reverse hyperglycaemia in mouse models of T1D by attenuating the autoimmune attack coupled to beta cell survival/regeneration prompted us to investigate whether immune tolerisation could be translated to individuals with T1D by LRH-1/NR5A2 activation and improve islet survival.
Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from individuals with and without T1D and derived into various immune cells, including macrophages and dendritic cells.
Biomaterials
May 2025
Center for Molecular Imaging and Nuclear Medicine, State Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection, Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou 215123, China. Electronic address:
The cross-talk between lysosomes and mitochondria is crucial for keeping intracellular homeostasis and metabolic function, providing a promising approach for tumor therapy. Herein, we employed polyvinylpyrrolidone (PVP)-modified Cu-gallic acid (CuGA) complex nano-boosters for amplifying lysosomes-mitochondria cascaded damage, and thereby effectively inducing cuproptosis and pyroptosis of breast tumor cells to boost anti-tumor immunotherapy. The CuGA nano-boosters could hijack lysosomal iron to form a bimetallic catalyst Cu(Fe)GA in situ through ion-exchange reaction, and cause the release of Cu and metal ion dysregulation (i.
View Article and Find Full Text PDFCell Biochem Biophys
December 2024
Ege University, Faculty of Medicine, Medical Biology Department, Izmir, Turkey.
Lung cancer (LC) accounts for approximately 25% of all cancer cases, with 80-85% of these being non-small cell lung cancer (NSCLC). VS-5584 is a novel anti-cancer agent that specifically inhibits mTORC1/2 and class I PI3K isoforms. There is cross-talk between the PI3K-Akt-mTOR and WNT signaling pathways that are abnormally activated in NSCLC.
View Article and Find Full Text PDFNutrients
November 2024
Faculty of Medicine, "Carol Davila" University of Medicine and Pharmacy, 050474 Bucharest, Romania.
Introduction: From the observation of a negative relationship between UV-B exposure and cancer rates, we hypothesized that vitamin D (VD) may play a protective role in oncogenesis. Moreover, repurposing a well-known and relatively safe drug for conditions with dismal prospects, such as pancreatic ductal adenocarcinoma (PDAC), is a tempting idea. Thus, we aimed to summarize the current knowledge regarding the role of VD in the prevention and treatment of PDAC.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Integrated Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou, Gansu 730000, China; Center for Heart, Lanzhou University of the First Hospital, Lanzhou, Gansu 730030, China. Electronic address:
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