C4d deposition is considered to be evidence of antibody-mediated rejection. This study was conducted to compare C4d immunoreactivity between villitis of unknown etiology (VUE) and cytomegaloviral placentitis. C4d immunohistochemistry was performed in cases with VUE (n = 16) and cytomegaloviral placentitis (n = 5). Distinct, linear C4d immunoreactivity along the syncytiotrophoblast was found in all VUE cases. In cytomegaloviral placentitis, the intensity of C4d immunoreactivity along the syncytiotrophoblast was not prominent, but cytoplasmic C4d immunoreactivity of villous cytotrophoblasts was frequently observed. Further screening of the cases with placental infarcts (n = 5) demonstrated prominent C4d immunoreactivity in the chorionic villi adjacent to the infarct. We report the characteristic co-localization of VUE and C4d immunoreactivity. The overall findings in this study strongly suggest that the complement activation is a common mechanism of diverse placental injuries associated with rejection, infection, and ischemia.
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http://dx.doi.org/10.1016/j.placenta.2013.02.003 | DOI Listing |
Acta Neuropathol
February 2024
Division of Neuropathology and Neurochemistry, Department of Neurology, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria.
Anti-glial fibrillary acidic protein (GFAP) meningoencephalomyelitis (autoimmune GFAP astrocytopathy) is a new autoimmune central nervous system (CNS) disease diagnosable by the presence of anti-GFAP autoantibodies in the cerebrospinal fluid and presents as meningoencephalomyelitis in the majority of patients. Only few neuropathological reports are available and little is known about the pathogenic mechanisms. We performed a histopathological study of two autopsies and nine CNS biopsies of patients with anti-GFAP autoantibodies and found predominantly a lymphocytic and in one autopsy case a granulomatous inflammatory phenotype.
View Article and Find Full Text PDFPregnancy Hypertens
June 2023
Renal Medicine Department, Queen Elizabeth Hospital Birmingham, Birmingham, UK.
Objectives: Pre-eclampsia (PE) is a leading cause of obstetric morbidity, with no definitive therapy other than delivery. We aimed to compare complement markers in maternal and fetal circulation, and placental tissue, between women with PE and healthy pregnant controls.
Study Design: Maternal and umbilical cord blood was tested for iC3b, C3, C4, properdin, Ba and C5b-9, and placental tissue for C3d, C4d, C9 and C1q, from women with PE (n = 34) and healthy pregnant controls (n = 33).
Front Cell Neurosci
March 2023
Faculty of Medicine, Health and Life Sciences, Swansea University Medical School, Swansea, United Kingdom.
Background: The extent of cortical pathology is an important determinant of multiple sclerosis (MS) severity. Cortical demyelination and neurodegeneration are related to inflammation of the overlying leptomeninges, a more inflammatory CSF milieu and with parenchymal microglia and astroglia activation. These are all components of the compartmentalised inflammatory response.
View Article and Find Full Text PDFHum Pathol
September 2022
Institute of Liver Studies, King's College Hospital, London SE5 9RS, UK. Electronic address:
This study was aimed to examine the clinical utility and impact of the 2016 Banff criteria for acute antibody-mediated rejection (acute AMR) in patients with liver transplantation. Among adult patients with donor-specific antibody (DSA) assays performed between 2015 and 2020, cases with proved DSA (mean fluorescent index >2000) and matched liver biopsy available were reviewed. Among 55 patients identified, 28 (51%) had class I DSA, 45 (82%) had class II DSA and 18 (33%) had both.
View Article and Find Full Text PDFBrain Pathol
September 2022
Faculty of Medical, Health and Life Sciences, Swansea University, Swansea, UK.
The extent of grey matter demyelination and neurodegeneration in the progressive multiple sclerosis (PMS) brains at post-mortem associates with more severe disease. Regional tissue atrophy, especially affecting the cortical and deep grey matter, including the thalamus, is prognostic for poor outcomes. Microglial and complement activation are important in the pathogenesis and contribute to damaging processes that underlie tissue atrophy in PMS.
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