Influence of genetic polymorphism of innate immunity genes on the development of immune pathology
- Authors: Kazumian MA1,2, Teplyakova ED2,3,4, Vasilenok AV1,5
-
Affiliations:
- Medical College
- Rostov State Medical University
- Children’s City Polyclinic No. 4
- Department of Health
- Pirogov Russian National Research Medical University,
- Issue: Vol 100, No 6 (2019)
- Pages: 944-949
- Section: Reviews
- URL: https://bakhtiniada.ru/kazanmedj/article/view/15897
- DOI: https://doi.org/10.17816/KMJ2019-944
- ID: 15897
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Abstract
The article presents the literature review devoted to NOD2/CARD15 gene. Genetic variability affects the susceptibility and development of certain human diseases such as autoimmune diseases and infections, affecting numerous cellular processes, and thus modulating the response to environmental and internal factors. The NOD2/CARD15 gene plays a major role in the development and course of various diseases such as Grohn's disease, Blau syndrome, as well as the risk of developing severe complications of the “graft versus host” reaction after allogeneic stem cell transplantation. NOD (Nucleotide Oligomerization Domain) is the domain of nucleotide oligomerization. NOD-like receptors play an important regulatory role in the response on infectious agents and at activation of the adaptive immune response. It is known that the mechanism of action of NOD-like receptors is based on the response to the pathogen of associated molecular patterns mainly of bacterial origin, which leads to the formation and activation of inflammasome. Recently, another NOD-like receptor activation mechanism has been revealed that provides innate virus recognition. The review presents Toll-like receptors, which are part of the innate immune system. Innate immunity is an inherited system of protection of the body against pathogenic and non-pathogenic microorganisms. The mechanisms of innate immunity develop very quickly. In newborns, the immune system is mainly dependent on components of the innate or antigen-independent immune system including phagocytes, natural killer cells, antigen-presenting cells, humoral inflammatory mediators and complement system.
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##article.viewOnOriginalSite##About the authors
M A Kazumian
Medical College; Rostov State Medical University
Author for correspondence.
Email: kazumianm@yandex.ru
SPIN-code: 5319-9946
Russian Federation, Moscow, Russia; Rostov-on-Don, Russia
E D Teplyakova
Rostov State Medical University; Children’s City Polyclinic No. 4; Department of Health
Email: elenatepl@rambler.ru
SPIN-code: 5864-9883
Russian Federation, Rostov-on-Don, Russia; Rostov-on-Don, Russia; Rostov-on-Don, Russia
A V Vasilenok
Medical College; Pirogov Russian National Research Medical University,
Email: aleksdokk@mail.ru
SPIN-code: 4753-5447
Russian Federation, Moscow, Russia; Moscow, Russia
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