Infection of mice by murine gammaherpesvirus 68 (MHV-68) represents a suitable animal model in which to investigate the immune response against gammaherpesviruses and to test the efficacy of vaccination strategies. In this study, we evaluated the efficacy of heat-inactivated MHV-68 as a vaccine as well as the adjuvant activity of type I interferon (IFN-I) administered together with the vaccine. Mice vaccinated with inactivated MHV-68 and subsequently infected with the virus exhibited a significant augmentation of the virus-specific humoral immune response and a considerable inhibition of MHV-68 acute replication in the lungs compared with unvaccinated control mice. The coadministration of IFN-I with inactivated MHV-68 significantly enhanced the humoral immune response elicited by the vaccine by stimulating the production of virus-specific IgG2 antibodies but did not significantly enhance protection from viral challenge. We conclude that IFN-I, recently shown to exhibit a powerful adjuvant activity to a poorly immunogenic subunit vaccine in mice, can also enhance the humoral immune response when used as adjuvant of an inactivated viral vaccine, even though this effect is less marked as a result of the strong immune response elicited by the inactivated virus alone, which may also involve the contribution of endogenous IFN.
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http://dx.doi.org/10.1089/10799900260442502 | DOI Listing |
Noise Health
January 2025
Department of Geriatric Health Internal Medicine, Qingdao Municipal Hospital, Qingdao 266000, China.
Objective: Evaluate the effect of white noise intervention on sleep quality and immunological indicators of patients with breast cancer undergoing neoadjuvant chemotherapy (NAC).
Methods: From January 2020 to December 2022, 104 newly diagnosed female patients (the number of people who met the inclusion criteria) with breast cancer who were confirmed to be preoperative NAC by puncture pathology were selected for a randomised single-blind trial. The patients were randomly divided into an observation group and a control group, with 52 cases in each group.
Br J Dermatol
January 2025
Division of Infection & Immunity, Cardiff University, Cardiff, UK.
Am J Physiol Endocrinol Metab
January 2025
National Agri-Food and Biomanufacturing Institute (BRIC-NABI), Food & Nutrition Biotechnology Division, S.A.S Nagar, Sector 81 (Knowledge City), Punjab, India.
Neuroimmunometabolism describes how neuroimmune cells, such as microglia, adapt their intracellular metabolic pathways to alter their immune functions in the CNS. Emerging evidence indicates that neurons also orchestrate the microglia mediated immune response through neuro-immune crosstalk perhaps through metabolic signalling. However, little is known about how the brain's metabolic microenvironment and microglial intracellular metabolism orchestrate the neuroimmune response in healthy and diseased brains.
View Article and Find Full Text PDFScience
January 2025
NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, CA, USA.
The metabolic landscape of cancer greatly influences antitumor immunity, yet it remains unclear how organ-specific metabolites in the tumor microenvironment influence immunosurveillance. We found that accumulation of primary conjugated and secondary bile acids (BAs) are metabolic features of human hepatocellular carcinoma and experimental liver cancer models. Inhibiting conjugated BA synthesis in hepatocytes through deletion of the BA-conjugating enzyme bile acid-CoA:amino acid -acyltransferase (BAAT) enhanced tumor-specific T cell responses, reduced tumor growth, and sensitized tumors to anti-programmed cell death protein 1 (anti-PD-1) immunotherapy.
View Article and Find Full Text PDFCancer Immunol Res
January 2025
University of Padua, Padua, PD, Italy.
T cell-based therapies, including Tumor Infiltrating Lymphocyte Therapy (TIL), T cell receptor engineered T cells (TCR T), and Chimeric Antigen Receptor T cells (CAR T), are powerful therapeutic approaches for cancer treatment. While these therapies are primarily known for their direct cytotoxic effects on cancer cells, accumulating evidence indicates that they also influence the tumor microenvironment (TME), by altering the cytokine milieu and recruiting additional effector populations to help orchestrate the antitumor immune response. Conversely, the TME itself can modulate the behaviour of these therapies within the host by either supporting or inhibiting their activity.
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