ESPN 51th Annual Meeting

ESPN 2018


 
Peculiarities of the immune system genes expression in steroid resistant nephrotic syndrome.
Sergey Morozov 1 Vladimir Dlin 1

1- ACADEMICIAN YU.E. VELTISHCHEV RESEARCH CLINICAL INSTITUTE OF PEDIATRICS, N.I. PIROGOV RUSSIAN NATIONAL RESEARCH MEDICAL UNIVERSITY, MINISTRY OF HEALTH OF THE RUSSIAN FEDERATION, MOSCOW, RUSSIA
 
Introduction:

Among cases of glomerulonephritis in children, patients with steroid-resistant nephrotic syndrome (SRNS) have the most unfavorable course, and the severity of the disease often determines immunological disorders. The study of the violations of the immune system genes expression will help to supplement knowledge of the pathogenesis of the SRNS development.

Material and methods:

28 children with SRNS at the age of 11 ± 4.05 years were examined, the control group consisted of 24 practically healthy children 13 ± 3.95 years of age. In the analyzed groups the expression of 614 immune system genes was analyzed on an nCounter digital nucleic acid analyzer (Nanostring Technologies, USA). 

Results:

 According to the data obtained, there is a low expression of genes of KIR Inhibiting Subgroup 1 – 18.4 ± 15.8 cu; KIR Inhibiting Subgroup 2 – 6.3 ± 5.5 cu; KIR3DL1 – 4.2 ± 3.6 cu, which is significantly lower than in the control group P – 0.01; P – 0.003; P – 0.02 (P < 0.05), respectively. The KIR genes family represents transmembrane glycoproteins localized on the plasma membrane that are involved in the formation of NK cells and T lymphocytes and interact with human leukocyte antigen (HLA) I class molecules that are expressed on all types of nuclear cells. KIR receptors identify and detect virus-infected or transformed cells.

High expression of the HLA-DPA gene (HLA class II) is noted – 1058 ± 411 cu, which is significantly higher than in the control group P – 0.001 (P < 0.05). HLA class II molecules are recognized primarily by CD4 + T helper cells. These lymphocytes increase the antigen-presenting function of the cells and promote the differentiation and proliferation of B cells and cytotoxic T lymphocytes.

Conclusions:

Thus, a decrease in the expression of transmembrane glycoproteins family genes that interact with first-class molecules of human leukocyte antigen (HLA) I and a significant increase in the expression of HLA class II genes can underlie the development of the SRNS pathogenesis and determine its severity.