Objective: Huntington’s Disease (HD) is a severe neurodegenerative disorder main pathogenic factor is CAG repeats in a suffered patients genome. Experimental therapy on the model of this disease and immunology evaluation was a goal of this research.

Background: We studied the comparative effects of experimental molecular and cell therapy with pluripotent stem neuronal cells in a mouse R7 /3 Huntington’s disease model. The transcription factor Elk-2 played a significant role in the formation of choreic hyperkinesis in these animals. In particular, neural stem cells (NSCs) for the treatment of HD have been developed from various sources, such as the brain itself, pluripotent stem cells (PSC), and somatic cells of patients with hypertension.

Method: The stem cell transplantation strategy for treating HD as a genetic disease is to replace dysfunctional or lost neurons; correction of mutant genes containing extended CAG repeats is necessary. Our approach to gene therapy based on the delivery of an enzyme that limits the rate of decomposition of cholesterol in the brain counteracts the many harmful effects of mutated huntingtin and has a stable neuroprotective effect in Huntington’s disease.

Results: A study of immune homeostasis revealed an optimization of the cytokine status indices in the HD model under the influence of experimental cell therapy. There was a restoration of IL-18 to 212, 51 + _27.42 pg / ml, the plasma concentration of antibodies to interferon alpha to 0.87 + _0.31 pg / ml, a slight decrease in the fine fraction (to 52.41 + _ 14, 82 conventional units and an increase in the large fraction of circulating immune complexes to 12, 43 + _4.65 units.
The immunomodulating properties of this type of treatment were manifested in relation to the activation of nonspecific immune reactions in the form of an increase in the phagocytic and metabolic function of neutrophilic granulocytes in relation to latex particles up to 87.52 + _11.23% and in the test with nitro blue tetrazolium which increased to 14, 73 + _4.52 %, neutrophil activation index in this case was equal to 4.82 + _1.49 units.

Conclusion: Immunololpgic properies of neurodegenerative disorders during experimental model treatment need further research and evaluation.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/cytokines-and-brain-specific-antibodies-in-experimental-cellular-and-molecular-treatment-of-huntingtons-diseases/