Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by loss of T cell tolerance to nuclear antigens. Studies in mice and humans have demonstrated that T cells from individuals with lupus are abnormal. Here, we review the known T cell defects in lupus and their possible biochemical nature, genetic causes, and significance for lupus pathogenesis.
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| http://dx.doi.org/10.1111/j.1749-6632.2003.tb06033.x | DOI Listing |
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NHC Key Laboratory of Hormones and Development, Chu Hsien-I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Background: In acute and chronic renal inflammatory diseases, the activation of inflammatory cells is involved in the defect of erythropoietin (EPO) production. Ras guanine nucleotide-releasing protein-4 (RasGRP4) promotes renal inflammatory injury in type 2 diabetes mellitus (T2DM). Our study aimed to investigate the role and mechanism of RasGRP4 in the production of renal EPO in diabetes.
View Article and Find Full Text PDFAdult patients with Philadelphia chromosome positive acute lymphoblastic leukemia undergoing allogeneic hematopoietic stem cell transplantation and tyrosine kinase inhibitors: development and validation of a clinical prediction model based on cytogenetics, IKZF1 deletions and minimal residual disease.
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Bone Marrow Transplantation Center, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310000, China.
The aim of this study was to develop and validate a nomogram predicting progression-free survival (PFS) for adult patients with positive acute lymphoblastic leukemia(Ph + ALL) who have undergone allogeneic hematopoietic stem cell transplantation(allo-HSCT) and tyrosine kinase inhibitor(TKI) treatment. Data were retrospectively collected from 176 adult patients diagnosed with Ph + ALL and treated with allo-HSCT and TKIs at The First Affiliated Hospital, Zhejiang University School of Medicine, between January 2015 and May 2023. 70% of the patients were randomly assigned to the training group(n = 124) and 30% of the patients were assigned to the validation group(n = 52).
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Division of Cell Therapy, Chiba Cancer Center Research Institute, Chiba, Japan.
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Institute of Biochemistry and Molecular Biology, Faculty of Medicine, University of Bonn, Bonn, Germany.
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View Article and Find Full Text PDFDysregulation of REST and its target genes impacts the fate of neural progenitor cells in down syndrome.
Sci Rep
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Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang, 43400, Selangor, Malaysia.
Increasing shreds of evidence suggest that neurogenic-to-gliogenic shift may be critical to the abnormal neurodevelopment observed in individuals with Down syndrome (DS). REST, the Repressor Element-1 Silencing Transcription factor, regulates the differentiation and development of neural cells. Downregulation of REST may lead to defects in post-differentiation neuronal morphology in the brain of the DS fetal.
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