The Fc-receptor function of macrophages and monocytes was studied in 10 healthy subjects and 10 patients (5 in phase of clinical activity) affected by systemic vasculitis with histological evidence of renal involvement. Macrophage function was detected by measuring the clearance in vivo of IgG-sensitized 51Cr-labelled autologous red blood cells (RBC). In vitro immune phagocytosis of monocytes was analysed as a kinetic phenomenon by incubating IgG-coated RBC with nearly pure suspensions of peripheral monocytes. All 5 patients studied in phase of clinical activity showed a defective Fc-receptor function in both the assays, as compared with normal subjects. Since a good correlation was found between the in vitro and the in vivo methods, the use of this non-invasive in vitro procedure is proposed as a substitute for the radioactive in vivo techniques in monitoring the course of the above disease.
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Hum Vaccin Immunother
December 2025
Department of Research and Development, ManySmart Therapeutics, Taipei, Taiwan.
Monoclonal antibodies enhance innate immunity, while bispecific T cell engager antibodies redirect adaptive T cell immunity. To stimulate both innate and adaptive mechanisms, we created a bifunctional eCD16A/anti-CD3-BFP adapter protein for combined use with clinically approved monoclonal IgG1 antibodies. The adaptor protein contains the extracellular domain of the human CD16A high-affinity variant, which binds the Fc domain of IgG1 antibodies, and an anti-human CD3 single-chain variable fragment that redirects T cell cytotoxicity.
View Article and Find Full Text PDFCell Mol Life Sci
January 2025
School of Basic Medical Sciences, Xinxiang Medical University, #601 Jinsui Road, Xinxiang, 453003, Henan, China.
Herpes simplex virus type I (HSV-1) infection is associated with lung injury; however, no specific treatment is currently available. In this study, we found a significant negative correlation between FcRn levels and the severity of HSV-1-induced lung injury. HSV-1 infection increases the methylation of the FcRn promoter, which suppresses FcRn expression by upregulating DNMT3b expression.
View Article and Find Full Text PDFFront Immunol
January 2025
Innovation Institute for Artificial Intelligence in Medicine and Zhejiang Provincial Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Introduction: Though COVID-19 as a public health emergency of international concern (PHEIC) was declared to be ended by the WHO, it continues to pose a significant threat to human society. Vaccination remains one of the most effective methods for preventing COVID-19. While most of the antigenic regions are found in the receptor binding domain (RBD), the N-terminal domain (NTD) of the S protein is another crucial region for inducing neutralizing antibodies (nAbs) against COVID-19.
View Article and Find Full Text PDFJ Immunother Cancer
January 2025
Center for Translational Research in Hematologic Malignancies, Houston Methodist Neal Cancer Center, Houston Methodist Research Institute, Houston, Texas, USA
Background: Cancer immunotherapy using immune checkpoint blockade (ICB) has revolutionized cancer treatment. However, patients with multiple myeloma (MM) rarely respond to ICB. Accumulating evidence indicates that the complicated tumor microenvironment (TME) significantly impacts the efficacy of ICB therapy.
View Article and Find Full Text PDFPLoS One
January 2025
Immunology and Immunotherapy Division, Center of Molecular Immunology (CIM), Havana, Cuba.
SARS-CoV-2 has continued spreading around the world in recent years since the initial outbreak in 2019, frequently developing into new variants with greater human infectious capacity. SARS-CoV-2 and its mutants use the angiotensin-converting enzyme 2 (ACE2) as a cellular entry receptor, which has triggered several therapeutic strategies against COVID-19 relying on the use of ACE2 recombinant proteins as decoy receptors. In this work, we propose an ACE2 silent Fc fusion protein (ACE2-hFcLALA) as a candidate therapy against COVID-19.
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