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Regulation of cardiac allograft immune responses by microRNA-155.
Transpl Immunol
December 2024
Norton Thoracic Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, United States of America. Electronic address:
Introduction: A better understanding of the immune mechanisms involved in allograft rejection after transplantation is urgently needed to improve patient outcomes. As microRNA-155 (miR155) plays a critical role in inflammation, we postulated that a deficiency of miR155 will improve cardiac allograft survival and enhance tolerance induction after heart transplantation.
Methods: We developed an acute rejection mouse model through heterotopic BALB/c cardiac transplantation to C57BL/6 (wild-type) and C57BL/6 miR155 knock-out (miR155KO) mice.
Co-stimulatory pathway competitive assay development using Liquid chromatography-tandem mass spectrometry (LC-MS/MS).
J Pharm Biomed Anal
May 2024
Department of Chemistry, Université du Québec à Montréal, Montreal, QC H3C 3P8, Canada. Electronic address:
T-cells play a significant role in the development of autoimmune diseases. The CD28-B7 costimulatory pathway is crucial for activating T-cells, and blocking this pathway is essential for treating autoimmune diseases. Therapeutic antibodies and fusion proteins that target costimulatory molecules like CD80, CD86, CTLA-4, and CD28 have been developed to explore the costimulation process and as targeted treatments.
View Article and Find Full Text PDFSuppression of the CD28/B7 pathway reduces the occurrence and development of myasthenia gravis and cytokine levels.
Int J Neurosci
September 2021
Department of Vascular Surgery, The First Affiliated Hospital of Hebei North University, Zhangjiakou, P. R. China.
Background: Myasthenia gravis (MG) is an antibody-mediated, autoimmune neuromuscular disease. Reports have indicated that the CD28/B7 ligand interactions play a crucial role during primary immune responses. Hence, the aim of the present study was to investigate the possible effects of the CD28/B7 pathway on the occurrence and development of MG and its associated cytokine factors.
View Article and Find Full Text PDFAs new members of the CD28/B7 costimulatory superfamily, PD-1 (programmed cell death 1) and its ligand PD-L1 (programmed cell death ligand 1) mediate a negative costimulatory signal, which inhibits functioning and proliferation of T and B cells, and reduce interleukin-2, interleukin-10, and interferon-γ secretion. This inhibitory pathway plays an important role in immune escape and the microenvironment of the tumor, and closely related to tumor progression. sPD-1 and sPD-L1 are the soluble form of PD-1 and PD-L1 in peripheral blood, which had not been well investigated.
View Article and Find Full Text PDFRescue of exhausted CD8 T cells by PD-1-targeted therapies is CD28-dependent.
Science
March 2017
Department of Microbiology and Immunology, Emory Vaccine Center, Emory University School of Medicine, Atlanta, GA 30322, USA.
Programmed cell death-1 (PD-1)-targeted therapies enhance T cell responses and show efficacy in multiple cancers, but the role of costimulatory molecules in this T cell rescue remains elusive. Here, we demonstrate that the CD28/B7 costimulatory pathway is essential for effective PD-1 therapy during chronic viral infection. Conditional gene deletion showed a cell-intrinsic requirement of CD28 for CD8 T cell proliferation after PD-1 blockade.
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