Objective: To observe the effects of chemokines CXCL9 and CXCL10 on cardiac allograft acute rejection mediated by alloreactive memory T cells in a retransplantation model.
Methods: Heart transplantation was performed 6 weeks after skin grafting. The mice were divided into 3 groups of control (direct heterotopic heart transplantation without skin grafting); experimental (heart transplantation after skin grafting) and syngraft (C57BL/6→C57BL/6, heterotopic heart transplantation) (n = 12 each). Graft survival and the pathological changes of cardiac graft were observed. And related gene expression in cardiac grafts and serum concentration of CXCL9/CXCL10 were detected.
Results: The mean survival time of control and experimental groups was 7.75 and 3.25 days respectively (P < 0.01).Serum concentrations of CXCL9 and CXCL10 in recipient mice were higher in the experimental group than those in the control group. Compared with the control group, the relative gene expressions of CXCL9 and CXCL10 were higher in the experimental group. According to pathological examinations, the histological rank of cardiac allograft was Grade 2.27 ± 0.25 in the control group versus Grade 4.12 ± 0.03 in the experimental group (P < 0.01).
Conclusions: CXCL9 and CXCL10 play critical roles in retransplantation mediated by alloreactive memory T cells. And acute rejection of cardiac allograft is more extensive in retransplantation.
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Int Immunopharmacol
January 2025
Department of Immunology, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, China. Electronic address:
Objective: Aberrant 6-phosphofructo-2kinase/fructose-2,6-bisphoshatase 3 (PFKFB3) expression is tightly correlated with multiple steps of tumorigenesis; however, the pathological significance of PFKFB3 in macrophages in patients with rheumatoid arthritis (RA) remains obscure. In this study, we examined whether PFKFB3 modulates macrophage activation and promotes RA development.
Method: Peripheral blood mononuclear cells (PBMCs) from patients with RA, THP-1 cells, and bone marrow-derived macrophages from conditional PFKFB3-knockout mice were used to investigate the mechanism underlying PFKFB3-induced macrophage regulation of RA.
Ann Clin Transl Neurol
January 2025
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA.
Defining the CSF cytokine/chemokine and injury biomarker signature of glial fibrillary acidic protein (GFAP) autoimmunity can inform immunopathogenesis. CSF GFAP-IgG-positive samples (N = 98) were tested for 17 cytokines/chemokines, neurofilament light chain (NfL), and GFAP (ELLA, Bio-Techne). Controls included non-inflammatory (N = 42), AQP4-IgG-positive (N = 83), CNS infections (N = 13), and neurosarcoidosis (N = 32).
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March 2025
Department of Dermatology, University Hospital of Zurich, University of Zurich, Schlieren, Switzerland.
In cutaneous melanoma, epigenetic dysregulation is implicated in drug resistance and tumor immune escape. However, the epigenetic mechanisms that influence immune escape remain poorly understood. To elucidate how epigenetic dysregulation alters the expression of surface proteins that may be involved in drug targeting and immune escape, we performed a 3-dimensional surfaceome screen in primary melanoma cultures and identified the DNA-methyltransferase inhibitor decitabine as significantly upregulating the costimulatory molecule ICAM-1.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Key Laboratory of Tropical Disease Control (Sun Yat-Sen University), Ministry of Education, Guangzhou, Guangdong, 510080, China.
Angiostrongylus cantonensis (AC) is the leading cause of eosinophilic meningoencephalitis worldwide. The neuroimmune interactions between peripheral and central immune systems in angiostrongyliasis remain unclear. In this study, significant infiltration of eosinophils, myeloid cells, macrophages, neutrophils, and Ly6C monocytes is observed in the brains of AC-infected mice, with macrophages being the most abundant.
View Article and Find Full Text PDFImmunohorizons
January 2025
Section of Infectious Diseases and Epidemiology, Department of Pediatrics, University of Colorado, Aurora, CO, United States.
Respiratory syncytial virus (RSV) is a major contributor to morbidity and mortality in infants. We developed an in vitro model of human respiratory infection to study cellular immune responses to RSV in infants, children, and adults. The model includes human lung epithelial A549 cells or human fetal lung fibroblasts infected with a clinical strain of RSV at a multiplicity of infection of 0.
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