Immunopathogenesis of inflammatory bowel diseases

The aim of review. To present analysis of data on immunopathogenesis of inflammatory bowel diseases.Key points. At genetically sensitive animals inflammatory bowel diseases (IBD) develop at various effects on innate and adaptive systems of immune defense (knock-out and transgenic mice), causing chan...

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Main Authors: Ye. A. Konovich, I. L. Khalif, M. V. Shapina
Format: Article
Language:Russian
Published: Gastro LLC 2013-09-01
Series:Российский журнал гастроэнтерологии, гепатологии, колопроктологии
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Online Access:https://www.gastro-j.ru/jour/article/view/1221
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author Ye. A. Konovich
I. L. Khalif
M. V. Shapina
author_facet Ye. A. Konovich
I. L. Khalif
M. V. Shapina
author_sort Ye. A. Konovich
collection DOAJ
description The aim of review. To present analysis of data on immunopathogenesis of inflammatory bowel diseases.Key points. At genetically sensitive animals inflammatory bowel diseases (IBD) develop at various effects on innate and adaptive systems of immune defense (knock-out and transgenic mice), causing changes of expression of significant immunologic factors with distortion of pro- and anti-inflammatory cells and molecules ratio at their contact to microbiota structures. The physiological state of intestine is characterized by balanced interaction of effector (Th1, Th2, Th17) and regulatory (Treg) cells determining presence of immune tolerance to resident microflora antigens. Innate immunity changes revealed in last years, related to mutations of genes of bacterial structures receptors (NOD2, toll-like receptors, autophagy), cause disorder of endocellular signal processes and pathological activation of cells of adaptive immunodefense of intestinal mucosa and conforming profile of cytokines with development of chronic inflammation which will be mediated: at Crohn's disease – by Th1-and Th17-cells, cytokines IL-12, interferon-γ etc., at ulcerative colitis – by Th2-and NKT-cells, cytokines IL-4 and IL-3 in combination to incompetence of suppressor function of regulatory Т-cells and their cytokines TGF-β (transforming growth factor) and IL-10.Conclusion. Investigations of experimental enterocolites and human IBD confirm immunologic hypothesis of pathogenesis: relation of their development to defects of innate and adaptive immune system.
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spelling doaj-art-9321ee2fc2f34902af11ecd304a51c3b2025-02-10T16:14:33ZrusGastro LLCРоссийский журнал гастроэнтерологии, гепатологии, колопроктологии1382-43762658-66732013-09-012346978803Immunopathogenesis of inflammatory bowel diseasesYe. A. Konovich0I. L. Khalif1M. V. Shapina2Federal state-funded institution «State Scientific Center of Coloproctology» Ministry of healthcare of the Russian FederationFederal state-funded institution «State Scientific Center of Coloproctology» Ministry of healthcare of the Russian FederationFederal state-funded institution «State Scientific Center of Coloproctology» Ministry of healthcare of the Russian FederationThe aim of review. To present analysis of data on immunopathogenesis of inflammatory bowel diseases.Key points. At genetically sensitive animals inflammatory bowel diseases (IBD) develop at various effects on innate and adaptive systems of immune defense (knock-out and transgenic mice), causing changes of expression of significant immunologic factors with distortion of pro- and anti-inflammatory cells and molecules ratio at their contact to microbiota structures. The physiological state of intestine is characterized by balanced interaction of effector (Th1, Th2, Th17) and regulatory (Treg) cells determining presence of immune tolerance to resident microflora antigens. Innate immunity changes revealed in last years, related to mutations of genes of bacterial structures receptors (NOD2, toll-like receptors, autophagy), cause disorder of endocellular signal processes and pathological activation of cells of adaptive immunodefense of intestinal mucosa and conforming profile of cytokines with development of chronic inflammation which will be mediated: at Crohn's disease – by Th1-and Th17-cells, cytokines IL-12, interferon-γ etc., at ulcerative colitis – by Th2-and NKT-cells, cytokines IL-4 and IL-3 in combination to incompetence of suppressor function of regulatory Т-cells and their cytokines TGF-β (transforming growth factor) and IL-10.Conclusion. Investigations of experimental enterocolites and human IBD confirm immunologic hypothesis of pathogenesis: relation of their development to defects of innate and adaptive immune system.https://www.gastro-j.ru/jour/article/view/1221inflammatory bowel diseasesimmunopathogenesisinnate and adaptive immunodefensepilot models
spellingShingle Ye. A. Konovich
I. L. Khalif
M. V. Shapina
Immunopathogenesis of inflammatory bowel diseases
Российский журнал гастроэнтерологии, гепатологии, колопроктологии
inflammatory bowel diseases
immunopathogenesis
innate and adaptive immunodefense
pilot models
title Immunopathogenesis of inflammatory bowel diseases
title_full Immunopathogenesis of inflammatory bowel diseases
title_fullStr Immunopathogenesis of inflammatory bowel diseases
title_full_unstemmed Immunopathogenesis of inflammatory bowel diseases
title_short Immunopathogenesis of inflammatory bowel diseases
title_sort immunopathogenesis of inflammatory bowel diseases
topic inflammatory bowel diseases
immunopathogenesis
innate and adaptive immunodefense
pilot models
url https://www.gastro-j.ru/jour/article/view/1221
work_keys_str_mv AT yeakonovich immunopathogenesisofinflammatoryboweldiseases
AT ilkhalif immunopathogenesisofinflammatoryboweldiseases
AT mvshapina immunopathogenesisofinflammatoryboweldiseases