Adaptive Immune Response Report
After any injury, it is a natural response that the immune system will trigger it inane or adaptive immune to protect or limit the injury to it body. The adaptive immune response is antigen-specific and requires the recognition of specific "non-self" antigens during a process called antigen presentation. B cells and T cells are the major types of lymphocytes in the immune system. However, when an adaptive immune response develops against self-antigens autoimmune response occurs with the characteristic representation of specific autoantibody generation. The CNS autoimmune response is more complex since CNS is considered as immune privileged site with a hiding behind selectively permeable physical blood-brain barrier (BBB) that provides an adaptation
to protect its delicate structures from the potential damage and irreversible effects of local immune activation and infiltration of circulating immune cells. Although several physiological characteristics of the CNS were thought to underlie the slow immune reactions in the brain in addition to the presence of the BBB, either brain-specific antigens or immune cells cross the barrier, is one of the majority requirements to trigger the autoimmune response. The BBB is formed by the brain endothelial cells connected by tight junctions. It is now becoming clear that neurons, astrocytic glia, pericytes, microglia and microvessels are organized into well-structured neurovascular or gliovascular units and these close cell-cell associations play important roles on the normal function of the BBB and the BBB phenotype of brain endothelial cells. The primary injury from TBI leads to mechanical dysfunction of the vascular and increased permeability of the BBB associated with brain cell damage, which further affect functional changes at the BBB. During the post-traumatic status, the first leakage of BBB coincides with increased production of a number of putative factors that may contribute to dysfunction of the BBB also. In addition, neuroinflammtion forces brain cell death cascade processes, endothelial cell damage or tight junction changes, which consistently affect BBB permeability. Functional changes of the BBB cause potential brain antigens to enter the systemic circulation as “foreigners” that lead to the initiation of an autoimmune response. When an adaptive immune response against self-antigens is not able to fulfill clearance processes, then autoreactive B cells are activated and differentiate into plasma cells that begin producing antibodies
to protect its delicate structures from the potential damage and irreversible effects of local immune activation and infiltration of circulating immune cells. Although several physiological characteristics of the CNS were thought to underlie the slow immune reactions in the brain in addition to the presence of the BBB, either brain-specific antigens or immune cells cross the barrier, is one of the majority requirements to trigger the autoimmune response. The BBB is formed by the brain endothelial cells connected by tight junctions. It is now becoming clear that neurons, astrocytic glia, pericytes, microglia and microvessels are organized into well-structured neurovascular or gliovascular units and these close cell-cell associations play important roles on the normal function of the BBB and the BBB phenotype of brain endothelial cells. The primary injury from TBI leads to mechanical dysfunction of the vascular and increased permeability of the BBB associated with brain cell damage, which further affect functional changes at the BBB. During the post-traumatic status, the first leakage of BBB coincides with increased production of a number of putative factors that may contribute to dysfunction of the BBB also. In addition, neuroinflammtion forces brain cell death cascade processes, endothelial cell damage or tight junction changes, which consistently affect BBB permeability. Functional changes of the BBB cause potential brain antigens to enter the systemic circulation as “foreigners” that lead to the initiation of an autoimmune response. When an adaptive immune response against self-antigens is not able to fulfill clearance processes, then autoreactive B cells are activated and differentiate into plasma cells that begin producing antibodies