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• W2755801421 abstract "Immune response against pathogens or foreign bodies involves the activation and participation of multiple receptors and pathways. Of these the Toll-like receptors (TLRs) play a critical role in sensing both exogenous and endogenous signals that characterize infection and inflammation. While an optimum activation of TLRs is a prerequisite to mount immune responses against infection, a well-regulated negative signaling is also crucial to bring the immune responses to homeostatic level. In the context of autoimmune diseases, the negative signaling that restores homeostasis is somewhat aberrant; besides there is also a constant supply of endogenous autoreactive danger molecules in the circulation or in the cytoplasm. Self-recognition that propels autoimmune diseases is blocked in normal physiology, where a highly regulated processing and intracellular lysosome-specific TLR9 activation specifically by the recognition of hypomethylated CpG is thought to ensure escape from self-recognition. However, a chronic activation of TLR and modification of cellular components by a synergistic participation of oxidative stress and global epigenetics are indicated for tissue damage and release of highly auto-reactive molecules in systemic lupus erythmatosus (SLE). This is accompanied by altered and dysfunctional innate and adaptive immune cells including T-lymphocytes that display altered methylation of genes that are necessary for immune regulation. Recent studies highlight a connection between intestinal commensal microbiota with TLR9-mediated modulation of innate and adaptive immune responses in the progression of autoimmune diseases. This indicates a role for diet modulating intestinal microbial colonization, which may have a serious impact on immune responses. The present chapter discusses the molecular mechanism of regulation of TLR signaling with an emphasis on how environmental factors at the face of genetic predisposition may influence CpG-DNA/TLR9-signaling-mediated SLE pathogenesis." @default.
• W2755801421 created "2017-09-25" @default.
• W2755801421 creator A5050371754 @default.
• W2755801421 date "2018-01-01" @default.
• W2755801421 modified "2023-09-26" @default.
• W2755801421 title "Inflammation in Systemic Immune Diseases" @default.
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