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| Figure 2: Hypothesis of immune system activation in hypertension. Increases in products from damaged, stressed or necrotic cells and tissues have been described in hypertension. These products, acting as damageassociated molecular patterns (DAMPs), can be recognized by pattern recognizing receptors, such as Toll-like receptors (TLRs) on antigenpresenting cells (APCs). APCs will process the DAMPs and present them on major histocompatibility complex (MHC) molecules to T cells. In this context, interaction between MHC/antigen and the T-cell receptor (TCR), co-stimulated by the binding of B7 to CD28 will activate the T cell. Activated T cells, as well as APCs, will release cytokines and chemokines, causing inflammatory cell infiltration and increases in ROS. These events will cause damage of various targets, such as the blood vessels, heart, kidney and central nervous system, all of which are main regulators of blood pressure. The resulting blood pressure increase itself will lead to further damage and stress which will increase DAMP levels, generating a positive feedback loop where increasing tissue damage perpetuates pro-inflammatory responses leading to chronic inflammation, resulting in vascular dysfunction and renal damage which may cause and contribute to the maintenance of hypertension. |
