Overactivity of NK cells is not limited to cytotoxic function, whereas the increased IL-2-induced secretion of IFN-γ and TNF-α
from NK cells have also been reported in AD patients [34–36]. However, serum levels of IFN-γ and TNF-α were similar in AD patients and normal subjects [35, 36]. In contrast to cytokine release in NK cells, it has been shown that vascular endothelial growth factor (VEGF) secretion in AD patients was significantly decreased in AD patients compared to healthy individuals [37]. In addition to these reports that imply dysregulation of NK cells function, it is demonstrated that NK cells sensitivity to apoptosis is increased in AD patients and correlated with Bcl-2 anti-apoptotic expression [38]. However, it should be noted that there is a possibility that the involvement of NK cell in AD is not a defensive reaction, but it could be a result of progression of AD, which leads to the activation of https://www.selleckchem.com/products/OSI-906.html immune system [39–41]. To approve this hypothesis, we should perform a long-time cohort study in which NK cell frequency and function has been considered in different times and in different stages of disease, particularly in the patients with stable disease that their disease shift to progressive phase. It is also suggested
that abnormalities in NK cells may lead to autoimmune diseases [42]. Thus, it may be possible that NK cell dysfunction has been www.selleckchem.com/products/DAPT-GSI-IX.html supposed as an aetiological factor in AD patients. However, to prove this hypothesis, we should investigate in this field for a long-time on a large sample size. As both neuroprotective [43, 44] and neurodegenerative [45] effects of NK cells on neuron cells have been reported, it seems that understanding the precise role of NK cells in immunopathogenesis of AD needs to performance
of several in vivo studies on experimental models. However, it should be noted that study of NK cells in vivo is difficult which is in part due to the lack of mouse strains with selective NK cell deficiency. Surprisingly, in a limited number of studies with NK cell depletion in MS experimental models, it has been shown that NK cells are protective cells which inhibit autoreactive response of TH1 cell [46, 47]. Contrary to these reports, there is evidence that implies NK cells facilitate Interleukin-3 receptor experimental MS induction [48, 49] so that NK cells were accumulated in the CNS of experimental autoimmune encephalomyelitis (EAE)-induced Lewis rats at the peak of disease. Moreover, antibody-mediated depletion of NK cells exacerbates disease after priming encephalitogenic T cells and enhances IFN-γ secreting TH1 cells [21]. The regulatory role of NK cells on TH1 responses in EAE not only in CNS but also in periphery is also demonstrated [50]. Interestingly, the studies on MS patients have shown that the frequency and function of NK cells are deficient [51], which are similar to AD reports.
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