MECHANISMS OF CELLULAR CYTOTOXICITY INDUCTION IN GASTRIC MUCOSAL INFLAMMATION

Development and chronicity of inflammatory process in gastric mucosa may contribute to persistence of a number of microorganisms – Helicobacter (H.) pylori, Staphylococcus (S.) aureus, Candida species (spp.), Herpesvirus and others in the host organism. Many authors have recognized an important role...

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Autor principal:	L. V. Matveeva
Formato:	article
Lenguaje:	RU
Publicado:	SPb RAACI 2017
Materias:	t lymphocytes cell cytotoxicity interleukin interferon helicobacter pylori herpesvirus candida Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/7cecb852fde142268e43fc9827747ade
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spelling	oai:doaj.org-article:7cecb852fde142268e43fc9827747ade2021-11-18T08:03:46ZMECHANISMS OF CELLULAR CYTOTOXICITY INDUCTION IN GASTRIC MUCOSAL INFLAMMATION1563-06252313-741X10.15789/1563-0625-2017-6-673-682https://doaj.org/article/7cecb852fde142268e43fc9827747ade2017-12-01T00:00:00Zhttps://www.mimmun.ru/mimmun/article/view/1391https://doaj.org/toc/1563-0625https://doaj.org/toc/2313-741XDevelopment and chronicity of inflammatory process in gastric mucosa may contribute to persistence of a number of microorganisms – Helicobacter (H.) pylori, Staphylococcus (S.) aureus, Candida species (spp.), Herpesvirus and others in the host organism. Many authors have recognized an important role of T helper (Th) type 1 and regulatory T cells in evolvement of gastritis, whereas importance of cytotoxic T lymphocytes (CTLs) is still to be confirmed. This review presents analysis of available scientific data about induction mechanisms of cellular cytotoxicity in inflammatory process affecting gastric mucosa. Bacterial populations, depending on their density, are able to regulate expression of genes encoding synthesis of protein virulence factors, thus accelerating adaptation for changing environmental conditions. Upon receptor-mediated recognition of characteristic microbial structures, i.e., pathogen-associated molecular patterns (PAMPs) and danger signals altered by stress, or cellular structures damaged by infectious pathogens (DAMPs), transcription factors are activated, thus leading to production of early pro-inflammatory interleukins (IL), interferons (IFN) type I and induction of immune responses. It is shown that the antigens of H. pylori and Candida spp. promote infiltration of mucosa gastric by activated CD8+CTLs, and Herpesvirus induce a significant increase in the number of perforin-positive (Pr+) CD8+ and CD16+ cells, phenotypic changes in CD4+lymphocytes, with acquisition of direct cytolytic activity.L. V. MatveevaSPb RAACIarticlet lymphocytescell cytotoxicityinterleukininterferonhelicobacter pyloriherpesviruscandidaImmunologic diseases. AllergyRC581-607RUMedicinskaâ Immunologiâ, Vol 19, Iss 6, Pp 673-682 (2017)
institution	DOAJ
collection	DOAJ
language	RU
topic	t lymphocytes cell cytotoxicity interleukin interferon helicobacter pylori herpesvirus candida Immunologic diseases. Allergy RC581-607
spellingShingle	t lymphocytes cell cytotoxicity interleukin interferon helicobacter pylori herpesvirus candida Immunologic diseases. Allergy RC581-607 L. V. Matveeva MECHANISMS OF CELLULAR CYTOTOXICITY INDUCTION IN GASTRIC MUCOSAL INFLAMMATION
description	Development and chronicity of inflammatory process in gastric mucosa may contribute to persistence of a number of microorganisms – Helicobacter (H.) pylori, Staphylococcus (S.) aureus, Candida species (spp.), Herpesvirus and others in the host organism. Many authors have recognized an important role of T helper (Th) type 1 and regulatory T cells in evolvement of gastritis, whereas importance of cytotoxic T lymphocytes (CTLs) is still to be confirmed. This review presents analysis of available scientific data about induction mechanisms of cellular cytotoxicity in inflammatory process affecting gastric mucosa. Bacterial populations, depending on their density, are able to regulate expression of genes encoding synthesis of protein virulence factors, thus accelerating adaptation for changing environmental conditions. Upon receptor-mediated recognition of characteristic microbial structures, i.e., pathogen-associated molecular patterns (PAMPs) and danger signals altered by stress, or cellular structures damaged by infectious pathogens (DAMPs), transcription factors are activated, thus leading to production of early pro-inflammatory interleukins (IL), interferons (IFN) type I and induction of immune responses. It is shown that the antigens of H. pylori and Candida spp. promote infiltration of mucosa gastric by activated CD8+CTLs, and Herpesvirus induce a significant increase in the number of perforin-positive (Pr+) CD8+ and CD16+ cells, phenotypic changes in CD4+lymphocytes, with acquisition of direct cytolytic activity.
format	article
author	L. V. Matveeva
author_facet	L. V. Matveeva
author_sort	L. V. Matveeva
title	MECHANISMS OF CELLULAR CYTOTOXICITY INDUCTION IN GASTRIC MUCOSAL INFLAMMATION
title_short	MECHANISMS OF CELLULAR CYTOTOXICITY INDUCTION IN GASTRIC MUCOSAL INFLAMMATION
title_full	MECHANISMS OF CELLULAR CYTOTOXICITY INDUCTION IN GASTRIC MUCOSAL INFLAMMATION
title_fullStr	MECHANISMS OF CELLULAR CYTOTOXICITY INDUCTION IN GASTRIC MUCOSAL INFLAMMATION
title_full_unstemmed	MECHANISMS OF CELLULAR CYTOTOXICITY INDUCTION IN GASTRIC MUCOSAL INFLAMMATION
title_sort	mechanisms of cellular cytotoxicity induction in gastric mucosal inflammation
publisher	SPb RAACI
publishDate	2017
url	https://doaj.org/article/7cecb852fde142268e43fc9827747ade
work_keys_str_mv	AT lvmatveeva mechanismsofcellularcytotoxicityinductioningastricmucosalinflammation
_version_	1718422361988923392

MECHANISMS OF CELLULAR CYTOTOXICITY INDUCTION IN GASTRIC MUCOSAL INFLAMMATION

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