Little is known about immune cell infiltrate type in the kidney allograft of patients with chronic-active antibody-mediated rejection (c-aABMR). In this study, multiplex immunofluorescent staining was performed on 20 cases of biopsy-proven c-aABMR. T-cell subsets (CD3, CD8, Foxp3, and granzyme B), macrophages (CD68 and CD163), B cells (CD20), and natural killer cells (CD57) were identified and counted in the glomeruli (cells/glomerulus) and the tubulointerstitial (TI) compartment [cells/high-power field (HPF)]. In the glomerulus, T cells and macrophages were the dominant cell types with a mean of 5.5 CD3 cells/glomerulus and 4 CD68 cells/glomerulus. The majority of T cells was CD8 (62%), and most macrophages were CD68CD163 (68%). The TI compartment showed a mean of 116 CD3 cells/HPF, of which 54% were CD8. Macrophage count was 21.5 cells/HPF with 39% CD68CD163. CD20 cells were sporadically present in glomeruli, whereas B-cell aggregates in the TI compartment were frequently observed. Natural killer cells were rarely identified. Remarkably, increased numbers of CD3FoxP3 cells in the TI compartment were associated with decreased graft survival ( = 0.004). Renal allograft biopsies showing c-aABMR show a predominance of infiltrating CD8 T cells, and increased numbers of interstitial FoxP3 T cells are associated with inferior allograft survival.
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http://dx.doi.org/10.3389/fimmu.2019.03106 | DOI Listing |
FEBS Lett
December 2024
Chemical Resource Development Research Unit, RIKEN Center for Sustainable Resource Science, Wako, Japan.
FOXO3a is a transcription factor involved in cell growth inhibition and apoptosis. FOXO3a is localized in the cytoplasm in cancer cells, and its nuclear translocation by small molecules is expected to prevent cancer cell growth. In this study, we screened a fungal broth library in HeLa cells using fluorescently labeled FOXO3a and an AI-based imaging system.
View Article and Find Full Text PDFInt J Hyperthermia
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Oncology Department, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China.
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View Article and Find Full Text PDFRegen Med
December 2024
Medical Center for Molecular Biology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
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Mitodicure GmbH, Kriftel, Germany.
Background: Recent studies provide strong evidence for a key role of skeletal muscle pathophysiology in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In a 2021 review article on the pathophysiology of ME/CFS, we postulated that hypoperfusion and ischemia can result in excessive sodium and calcium overload in skeletal muscles of ME/CFS patients to cause mitochondrial damage. Since then, experimental evidence has been provided that supports this concept.
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December 2024
Cardiovascular Research Center, Massachusetts General Hospital, Boston. (C.C., P.X., Z.Y., Y.S., E.S.L., J.D.R., M.C.H.).
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