ANAT 322 Lecture Notes - Lecture 7: Nonsteroidal Anti-Inflammatory Drug, Aspirin, Endothelium
3 Sep 2016
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Document Summary
Body constantly needs to defend self against pathogens in environment. Then activate cellular & humoral innate immune response (e. g. phagocytosis, complement activation) 100 trillion bacteria in human body, we interact w/them. If bacteria enters body, innate molecular tools to recognize non-self. Tlr are specific, but no improvement over time. On cell-membrane (almost every cell type can express prr, but immune cells more reactive) trigger signalling cascades changes in gene expression of secondary mediators. Lipopolysaccharides (lps) in gram-negative bacteria cell wall; tlr4. Other types of tlr that recognize flagellin, dsrna, lipoproteins, unmethylated cpgs, etc. Nfkb: essential for all immune responses, also activated at subsequent levels. Sequestered in cytoplasm normally; when activated translocates into nucleus to directly control specific gene expression. Irf: activated by tlf & ifs, translocated to nucleus, control gene expression. One gene activated by tlr, then activate own receptors to perform diff functions. Soluble, exported out of cell into blood/icf & travel to other areas.
