Type I IFNs constitute a family of proteins exhibiting high homology in primary, secondary, and tertiary structures. They interact with the same receptor and transmit signals to cellular nucleus through a similar mechanism, eliciting roughly homogeneous biological activity. Nevertheless, the members of that family, IFN alpha species, IFN beta and IFN omega, due to local differences in the structure sometime show distinct properties. From the reported data it results that even minute changes or differences in the primary sequences could be responsible for a significant variety of biological actions, thus inducing to the hypothesis that Type I IFNs, rather than to be the result of a redundant replication during the evolution play definite roles in the defense of living organisms to foreign agents.
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http://dx.doi.org/10.1007/BF02678218 | DOI Listing |
Kidney Int Rep
January 2025
Translational Science and Experimental Medicine, Early R&I, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UK.
Type I interferons (IFNs) are immunostimulatory molecules that can activate the innate and adaptive immune systems. In cases of immune dysfunction, prolonged activation of the type I IFN pathway has been correlated with kidney tissue damage in a wide range of kidney disorders, such as lupus nephritis (LN) and focal segmental glomerulosclerosis (FSGS). Genetic mutations, such as risk variants in conjunction with elevated type I IFN expression, are also associated with higher rates of chronic kidney disease in patients with LN and collapsing FSGS.
View Article and Find Full Text PDFNanoscale
January 2025
Department of Oncology, Shanghai East Hospital, School of Medicine, Shanghai Key Laboratory of Chemical Assessment and Sustainability, School of Chemical Science and Engineering, Tongji University, Shanghai 200092, China.
The exclusion of immune cells from the tumor can limit the effectiveness of immunotherapy in triple negative breast cancer (TNBC). The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway plays a crucial role in priming adaptive anti-tumor immunity through the production of type I interferons (IFNs), facilitating the maturation of dendritic cells (DCs) and the function of T cells. Although the increased expression of programmed death-ligand 1 (PD-L1) upon STING activation is favorable for amplifying the efficacy of immune checkpoint inhibitors (ICIs) and realizing combination therapy, the penetration barrier remains a major obstacle.
View Article and Find Full Text PDFImmun Inflamm Dis
January 2025
Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Department of Public Health and Infectious Diseases, Sapienza University, Rome, Italy.
Background: Several respiratory viruses, including Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2), suppress nuclear factor-E2-related factor-2 (NRF2) antioxidant response, generating oxidative stress conditions to its advantage. NRF2 has also been reported to regulate the innate immune response through the inhibition of the interferon (IFN) pathway. However, its modulation in younger individuals and its correlation with the IFN response remain to be elucidated.
View Article and Find Full Text PDFRedox Biol
January 2025
Department of Pathogenic Biology, Key Laboratory of Infection and Immunity of Shandong Province, and Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China. Electronic address:
Cellular microenvironments critically control the activation of innate immune responses. N-chlorotaurine (Tau-Cl) is an endogenous metabolite that is markedly produced and secreted during pathogenic invasion. However, its effect on the antiviral innate immune responses remains unclear.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
School of Life Science and Technology, China Pharmaceutical University, Nanjing, China; Department of Biomedical Science, City University of Hong Kong, Kowloon, Hong Kong, China. Electronic address:
Cyclic GMP-AMP synthase (cGAS)-Stimulator of interferon genes (STING) signaling pathway, an essential element in the innate antiviral immune responses, has emerged as a key component of innate immune system to modulate type I IFNs production and response by recognizing both exogenous and endogenous DNA. Although some cGAS-STING signaling small molecule agonists have been developed, there are few natural polysaccharides reported to activate cGAS-STING signaling for the treatment of infectious diseases. Here, we reported that Laminaran, a low molecular weight β-glucan storage polysaccharide present in brown algae, potentiates cGAS-STING signaling to promote type I IFNs production and antiviral response.
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