Host defence comprising many biological structures and processes within an organism that protect against various diseases is known as immune system(97). Immune system can be classified broadly in two sub-systems, the innate immune system versus the adaptive immune system, or humoral immunity versus cell mediated immunity. In humans, the blood-brain barrier, blood-cerebrospinal fluid barrier separate peripheral immune system from the neuroimmune system which protects the brain(98). Malfunctioning of immune system can result in autoimmune diseases, inflammatory diseases and cancer.
Less active immune system results in life threatening infections and various immunodeficiencies. In humans, immunodeficiency can either be the result of a genetic
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Both defence mechanism of the immune system have ability to distinguish between self and non-self molecules. In immunology, self molecules are those components of an organism’s body that can be distinguished from foreign substances by the immune system (102), while non-self of molecules are those that are recognized as foreign molecules. One class of non-self molecules are called antigens and are defined as substances that bind to specific immune receptors and elicit an immune response(102).Non-specific defence mechanism is known as innate immune system, meaning these systems respond to pathogens in a generic way(99). No immunological memory is developed during innate immune response. The innate immune system is the dominant system of host defence in most organisms. When microbes are identified by pattern recognition receptors, which recognize components that are …show more content…
They instead control the immune response by directing other cells to perform these tasks. Helper T cells express T cell receptors (TCR) that recognize antigen bound to Class II MHC molecules. The MHC-antigen complex is also recognized by the helper cell’s CD4 co-receptor, which recruits molecules inside the T cell (e.g., KGA) that are responsible for the T cell’s activation. Helper T cells have a weaker association with the MHC-antigen complex than that observed for killer T cells, meaning many receptors (around 200–300) on the helper T cell must be bound by MHC-antigen in order to activate the helper cell, while killer T cells can be activated by engagement of a single MHC-antigen molecule. Helper T cell activation also requires longer duration of engagement with an antigen-presenting cell