China
Africa
Explore chapters and articles related to this topic
Systemic Lupus Erythematosus
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Vaneet K. Sandhu, Neha V. Chiruvolu, Daniel J. Wallace
DNA methylation is an epigenetic mechanism where a methyl group is transferred to the fifth carbon of the cytosine pyrimidine ring and involved in cell differentiation, silencing of transposable elements, and gene imprinting. UV light, hydralazine, and procainamide can inhibit DNA methylation, inciting SLE-like disease. One of the first studies on DNA methylation showed that suppressing this process in CD4+ T cells during mitosis led to formation of autoreactive CD4+ T cells. This was backed by more studies which revealed that expression of genes suppressed by DNA methylation can lead to T cell–mediated autoreactivity.83 Studies with microarrays have shown that hypomethylation of IFN genes such as MX1, BST2, and IFI44L can lead to SLE pathogenesis.50
HIV-1 infection in sickle cell disease and sickle cell trait: role of iron and innate response
Published in Expert Review of Hematology, 2022
SCD patients have higher levels of iron-regulatory, hypoxia-related and inflammatory proteins including significantly upregulated (>100-fold) FTL1, TLR4 (toll-like receptor 4), IL6 (interleukin-6) gene expression levels and higher levels of C-reactive protein [20]. SCD patients also have higher levels of anti-inflammatory IL-10 and pro-inflammatory IFN-γ, IL-6, IL-8 and RANTES cytokines [23]. As described in the previous section, SCD PBMCs express several interferon-inducible proteins, some of which can be induced by type 1 interferons (IFN-α/β). Recently, plasma heme levels in SCD patients were positively correlated with circulating levels of IFN-α and upregulation of the IFN-α/β inducible genes in circulating monocytes [22]. In mice treated with hemin, IFN-α/β expression occurred in liver monocyte and macrophages suggesting a novel IFN-α/β activating pathway mediated by hemolysis [22]. Among 12 subtypes of IFN-α, only IFN-α14 inhibits HIV-1 and induces expression of BST2, MX2 and APOBEC3G genes [107]. Expression of IFN-β by HIV-1 infected macrophages restricted HIV-1 infection [108]. Earlier studies also showed that transduction of macrophages with IFN-β – expressing retroviral vector led to HIV-1 resistance linked to the elevated expression of RANTES and downregulation of CCR5 co-receptor [109]. Interestingly, elevated levels of RANTES were detected in SCD patients’ plasma [23]. Taken together, SCD patients express both pro- and anti-inflammatory cytokines including type 1 and 2 interferons. Expression of some of the HIV-1 restriction factors that we and others observed in SCD PBMCs might be driven in part byIFN-α/β expression.
BST2 Promotes Tumor Growth via Multiple Pathways in Hepatocellular Carcinoma
Published in Cancer Investigation, 2020
Xiaoguang Xu, Yu Wang, Fangxi Xue, Encui Guan, Feng Tian, Jian Xu, Hongjin Zhang
Bone marrow stromal cell antigen 2 (BST2), also known as CD317, has been identified as a cell surface glycoprotein (5). It is a 35kD transmembrane protein composed of a cytoplasmic N-terminal region, a transmembrane domain, a coiled-coil extracellular region, and followed by a C-terminal glycosylphosphatidylinositol (GPI) anchor domain (6). BST2 was originally reported to serve as a specific surface marker of differentiated B cells (7). The expression of BST2 can be normally detected in mature and neoplastic B cells, dendritic cells and bone marrow stromal cells, but not on other cell types in the peripheral blood and different tissues such as stomach, liver, and spleen (8,9).