| Autor: |
Labudzynskyi DO, Manoylov KU, Shymanskyy IO, Veliky MM |
| Jazyk: |
English; Russian |
| Zdroj: |
TSitologiia i genetika [Tsitol Genet] 2016 Jul-Aug; Vol. 50 (4), pp. 38-49. |
| Abstrakt: |
The mechanisms of diabetes-associated impairment of cellular immune defense and its regulation by vitamin D3 are not fully elucidated. The study was devoted to investigating the functional state of T-cell immunity as well as humoral immune activity in response to artificial immunization in experimental diabetes and after prolonged administration of vitamin D3. It was established that diabetes is characterized by a 2.3 times decrease in blood serum 25OHD3 content. Vitamin D3 deficiency was accompanied by the failures in proliferative activity of T-lymphocytes and alterations of the regulatory (CD4+-postive lymphocytes) and cytotoxic (CD8+-positive lymphocytes) cell subpopulations. It was found an increase in the content of phosphorylated p65 subunit of nuclear factor κB in total lysates of spleen T lymphocytes and its enhanced translocation to the nucleus. In addition, it was shown intensification of humoral IgG response to administration of recombinant diphtheria toxin subunit B. Revealed impairments in the cellular link of the immune system were associated with an increase in splenocytes apoptosis, which was detected by Annexin V-GFP ability to bind phosphatidyl serine that is specifically located on the outer surface of plasmalemma in apoptosis. Prolonged vitamin D3 treatment (within 2 months) in a dose of 20 IU/animal leads to normalization of the proliferative activity and the ratio of T-cell subpopulations, reduces the formation of phosphorylated subunit of NF-κB - p65 and contributes to a balanced secretion of IgG against artificial antigen. These changes were accompanied by a decrease in apoptotic events in the total population of splenocytes. Our findings suggest an important role of vitamin D3 in the regulation of the immune system abnormalities related to type 1 diabetes. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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