Modern view on the role of pattern-recognition receptors and signaling pathways in the development of innate immunity in viral infections

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Abstract

Features of organization and functioning of pattern-recognizing receptors and signaling pathways in induction of antiviral immune response are considered. The recognition of antigenic structures of the virus is carried out by pathogen-associated molecular patterns of innate immunity cells. These are Toll-like receptors, nucleotide-binding oligomerization domain-like receptors, lectin C-type receptors, and RIG-I-like receptors. The functioning of these receptor structures depends on protein molecules that provide activation signals. These are the adapter proteins of the primary response of myeloid differentiation 88, interleukin-1 receptor-associated kinase, nuclear factor-KB. Interactions of cellular proteins in the activation of signaling pathways are complex and receptor-ligand reactions can lead to different outcomes in a single cell, in most cases leading to a limitation of viral reproduction. An important obstacle to the effective recognition of viruses and the development of an adequate immune response is the close organization of viral antigens and receptor structures of the cell. The role of LGP2 protein molecules is associated with the peculiarities of the development of the immune response, which can be not only positive, but also negative regulators of the transmission of excitation signals from intracellular cytoplasmic helicase receptors. A number of viral proteins inhibit activation signals, which ultimately leads to various options for the development of the immune response. A special role belongs to the transmembrane protein of the endoplasmic reticulum, which increases the expression of interferon β — a stimulator of interferon genes that provide detection of deoxyribonucleic acid viruses. Maximum activation of this protein, ensures the effective development of a cellular antiviral immune response.

About the authors

Alexander V. Moskalev

Military Medical Academy of S.M. Kirov

Email: alexmav195223@yandex.ru
ORCID iD: 0000-0002-3403-3850
SPIN-code: 8227-2647

Doctor of Medical Sciences, Professor

Russian Federation, Saint Petersburg

Boris Yu. Gumilevsky

Military Medical Academy of S.M. Kirov

Email: alexmav195223@yandex.ru
SPIN-code: 3428-7704
Scopus Author ID: 6602391269
ResearcherId: J-1841-2017

Doctor of Medical Sciences, Professor

Russian Federation, Saint Petersburg

Andrey V. Apchel

Military Medical Academy of S.M. Kirov

Author for correspondence.
Email: apchelvya@mail.ru
ORCID iD: 0000-0001-7658-4856
SPIN-code: 4978-0785
Scopus Author ID: 6507529350
ResearcherId: Е-8190-2019

Doctor of Medical Sciences, Professor

Russian Federation, Saint Petersburg

Vasiliy N. Tsygan

Military Medical Academy of S.M. Kirov

Email: vn-t@mail.ru
ORCID iD: 0000-0003-1199-0911
SPIN-code: 7215-6206

Doctor of Medical Sciences, Professor

Russian Federation, Saint Petersburg

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Supplementary files

Supplementary Files
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1. JATS XML
2. Fig. The cGAS/STING axis in innate immunity: double-stranded DNA in the cytoplasm (from microbes with DNA genomes, from the cell nucleus, or from damaged mitochondria) is detected by cyclic GMP-AMP (cGAMP) synthase (cGAS), which is activated to synthesize the cyclic dinucleotide cGAMP(2'–5') as its second messenger molecule (using the substrates ATP and GTP). cGAMP(2'–5') then binds to and activates the endoplasmic reticulum (ER)-resident receptor STING (stimulator of interferon genes). Activated STING translocates to a perinuclear Golgi compartment, where it binds to TBK1 (TANK-binding kinase 1) to activate IRF3 and induce NF-kB activation

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Copyright (c) 2022 Moskalev A.V., Gumilevsky B.Y., Apchel V.Y., Tsygan V.N.

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