The concept of stress supports the idea that the brain can control immune system activity. New advances in studying the central nervous system’s interactions with the immune system have revealed a large connectivity network between the two systems. Branches of the autonomic nervous system innervate lymphoid organs.
Most neurotransmitters and neuropeptides have membrane connections on accessory immune cells and lymphocytes. The engagement of these receptors causes changes in immunity functions such as cell proliferation, chimiotactisme, and individual immune responses. In addition, brain injuries and stress can affect the immune system’s function. The neuroendocrine system isn’t responsible for these changes.
They may also be depending on the function of the autonomic nervous system. Signals from the immune system normally activate communication routes between the brain and the immune system to control immune responses. These signals are mostly expressed by proinflammatory cytokines and occur from accessory immune cells such as macrophages and macrophages.
Proinflammatory cytokines from the periphery act on the brain via two main pathways:
(1) a humoral pathway that helps pathogen-specific molecular patterns to respond on Toll-like receptors in brain areas that lack a functional blood-brain barrier, the so-called core structures areas; and
(2) a neural pathway defined by afferent nerves that control muscle the bodily site of infection and injury. The expression of brain cytokines produced by resident macrophages and microglial cells increases by peripherally produced cytokines in both situations.
These generated cytokines diffuse all across the brain parenchyma, impacting specific brain areas to organize the host response (fever, neuroendocrine activation, and sickness behavior).
Scientists found that the brain’s immune systems are different. Outside tissue transferred into most body parts usually triggers an immune reaction; however, tissue grafted into the nervous system produces a much less hostile response.