In addition to stimulating factors such as cytokines which can provoke NK cells function, it should be noted that viral infections Autophagy Compound Library clinical trial may be as other potent
stimulators of NK cells in AD. It has been shown that CNS infections by herpes simplex virus type 1, picornavirus, Borna disease virus, and other microorganisms such as Chlamydia pneumonia, Helicobacter pylori, and spirochaete could be possible aetiological agents in the development of AD [62, 63]. AD is a progressive and neurodegenerative disorder that accounts for 50–60% of all dementia patients. It is characterized by language difficulties, impairments in decision-making and cognitive dysfunction. The responsible mechanisms in degeneration of cerebral neurons and synapses in AD remain an enigma.
The AD patients’ brain shows some degree of cerebral atrophy, but the extent of neuronal loss varies among patients. The Beta amyloid has been found outside senile plaques and within cerebral blood vessels in AD cases . Increased production of cytokines, such as IL-1α, IL-1β, IL-2, IL-3, IL-6, and TNF-α in senile plaques in the hippocampus and cortex of Alzheimer’s brain has been reported . NK cells are granular lymphocytes that have cytotoxic activities. They can affect adaptive immune responses Selleck Alectinib and control immune cell homoeostasis in humans Edoxaban and they can produce cytokines, such as IFN-γ, IL-3, IL-5, IL-10, IL-12 and IL-13 . Recent findings show that NK cells are involved in AD and could be a target for evaluating the immunopathogenesis of this disease and/or approaching to prevention and treatment of AD . Regarding the results of various studies, it seems that although the frequency of NK cells in AD is not affected, however, their functional potential shows some degree of defects [7, 32]. Surprisingly, it has been shown that this anergic behaviour of NK cells in AD patients is not permanent and their NK cells
can be a potent cytotoxic and cytokine secreting cells following cytokine-mediated stimulation . The cause of this behaviour is unknown but it is suggested that dysregulation in signalling pathways is in part involved in this fashion . The precise role of NK cells as protective or deleterious factors in AD immunopathogenesis is also matter of debate. However, knowing this matter that NK cells can be as a therapeutic target in AD therapy requires to more investigation in both human and its animal experimental models in the future. “
“During the past decade, it has been firmly established that IL-23 is essential for disease development in several models of autoimmune disease, including psoriatic skin inflammation, inflammatory bowel disease (IBD), and experimental autoimmune encephalomyelitis (EAE).