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Role of interferons in the antiviral battle: from virus-host crosstalk to prophylactic and therapeutic potential in SARS-CoV-2 infection.
Front Immunol
January 2024
Microbiology Immunology Department, Faculty of Biology, University of Bucharest, Bucharest, Romania.
Mammalians sense antigenic messages from infectious agents that penetrate the respiratory and digestive epithelium, as well as signals from damaged host cells through membrane and cytosolic receptors. The transduction of these signals triggers a personalized response, depending on the nature of the stimulus and the host's genetics, physiological condition, and comorbidities. Interferons (IFNs) are the primary effectors of the innate immune response, and their synthesis is activated in most cells within a few hours after pathogen invasion.
View Article and Find Full Text PDFThis article presents a retrospective analysis of the research findings by professor A.A. Kasparov, who developed and implemented a novel approach to treating ocular herpes.
View Article and Find Full Text PDFGenetic and Epigenetic Regulation of the Innate Immune Response to Gout.
Immunol Invest
April 2023
Microbiology, Parasitology and Pathology Program, Universidade Federal do Parana (UFPR), Curitiba, Brazil.
Gout is a disease caused by uric acid (UA) accumulation in the joints, causing inflammation. Two UA forms - monosodium urate (MSU) and soluble uric acid (sUA) have been shown to interact physically with inflammasomes, especially with the nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3), albeit the role of the immune response to UA is poorly understood, given that asymptomatic hyperuricemia does also exist. Macrophage phagocytosis of UA activate NLRP3, lead to cytokines release, and ultimately, lead to chemoattract neutrophils and lymphocytes to the gout flare joint spot.
View Article and Find Full Text PDFDistinct phenotypes and 'bystander' effects of senescent tumour cells induced by docetaxel or immunomodulatory cytokines.
Int J Oncol
November 2018
Laboratory of Immunological and Tumour Models, Institute of Molecular Genetics of the Czech Academy of Sciences, v.v.i., Prague 4 142 20, Czech Republic.
Cellular senescence is the process of the permanent proliferative arrest of cells in response to various inducers. It is accompanied by typical morphological changes, in addition to the secretion of bioactive molecules, including proinflammatory cytokines and chemokines [known as the senescence-associated secretory phenotype (SASP)]. Thus, senescent cells may affect their local environment and induce a so-called 'bystander' senescence through the state of SASP.
View Article and Find Full Text PDFRelease of interleukin-10 and neurotrophic factors in the choroid plexus: possible inductors of neurogenesis following copolymer-1 immunization after cerebral ischemia.
Neural Regen Res
October 2018
Centro de Investigación en Ciencias de la Salud (CICSA), FCS, Universidad Anáhuac México Norte, Huixquilucan, Estado de México, México.
Copolymer-1 (Cop-1) is a peptide with immunomodulatory properties, approved by the Food and Drug Administration of United States in the treatment of multiple sclerosis. Cop-1 has been shown to exert neuroprotective effects and induce neurogenesis in cerebral ischemia models. Nevertheless, the mechanism involved in the neurogenic action of this compound remains unknown.
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