Genes & CellsGenes & CellsГены и КлеткиGenes and Cells2313-18292500-2562Human Stem Cells Institute61025210.17816/gc610252ReviewsНаучные обзорыReview ArticleImmune cell balance as potential biomarker of progressing non-alcoholic fatty liver diseaseБаланс иммунных клеток как потенциальный биомаркёр прогрессирования неалкогольной жировой болезни печениhttps://orcid.org/0000-0001-8697-20865343-0984TopchievaLudmila V.ТопчиеваЛюдмила Владимировна
Russian Federation

Cand. Sci. (Biology)

канд. биол. наук

topchieva67@mail.ruhttps://orcid.org/0000-0001-7620-70652471-3111KurbatovaIrina V.КурбатоваИрина Валерьевна
Russian Federation

Cand. Sci. (Biology)

канд. биол. наук

irina7m@yandex.ruhttps://orcid.org/0000-0003-2613-56946034-5892DudanovaOlga P.ДудановаОльга Петровна
Russian Federation

MD, Dr. Sci. (Medicine), Professor

д-р мед. наук, профессор

odudanova@gmail.comhttps://orcid.org/0000-0003-3849-6796VasilevaAlina V.ВасильеваАлина Валерьевна
Russian Federation
kennard@inbox.ruhttps://orcid.org/0000-0001-6266-32899727-9972ZhulaiGalina A.ЖулайГалина Анатольевна
Russian Federation

Cand. Sci. (Biology)

канд. биол. наук

zhgali-111@yandex.ruInstitute of Biology of Karelian Research Centre Russian Academy of SciencesИнститут биологии Карельского научного центра РАНPetrozavodsk State UniversityПетрозаводский государственный университет05032024280320241911051251710202308022024Copyright ©; 2024, Eco-VectorCopyright ©; 2024, Эко-Вектор2024Eco-VectorЭко-Векторhttps://creativecommons.org/licenses/by-nc-nd/4.0/https://genescells.ru/2313-1829/article/view/610252

Nonalcoholic fatty liver disease (NAFLD) is a widespread chronic, slowly progressive metabolic multifactorial disease. It is represented by several clinical and morphological forms: steatosis, nonalcoholic steatohepatitis (NASH) (with or without fibrosis), and liver cirrhosis. The search for minimally invasive and cost-effective biomarkers of NAFLD is a key task in the diagnosis, staging of progression, and long-term monitoring of NAFLD. This article discusses the possibility of using immune cell balance as potential minimally invasive peripheral markers of NAFLD progression. In the progression of NASH from steatosis to fibrosis and cirrhosis, inflammation plays an important role because of the activation of Kupffer cells and increased migration of monocytes, dendritic cells, neutrophils, and activated T lymphocytes into the tissues. Macrophages originating from monocytes, with NASH progression, gradually begin to prevail over the pool of resident macrophages. The risk of NASH and fibrosis development in patients with NAFLD increases with the ratio of neutrophils/lymphocytes in the liver. An increase in the Th17 cell count and a decrease in T-regulatory cell count can contribute to increased hepatic steatosis and inflammation development in NAFLD and accelerate the transition from simple steatosis to steatohepatitis and fibrosis. Information on the participation of noncoding RNAs in the regulation of the balance of immune cells in NAFLD is presented, which also allows us to consider them as additional, along with cellular, markers of disease progression.

Неалкогольная жировая болезнь печени (НАЖБП) — широко распространённое хроническое, медленно прогрессирующее метаболическое многофакторное заболевание, представленное рядом клинико-морфологических форм: стеатозом, неалкогольным стеатогепатитом (НАСГ) (с фиброзом или без него) и циррозом печени. Поиск малоинвазивных и экономически эффективных биомаркёров НАЖБП является ключевой задачей в диагностике, стадировании прогрессирования и долгосрочном мониторинге НАЖБП. Обсуждается возможность использования баланса иммунных клеток в качестве потенциальных малоинвазивных периферических маркёров прогрессирования НАЖБП. В прогрессировании НАСГ (от стеатоза к фиброзу и циррозу) важную роль играет воспаление, реализующееся за счёт активации клеток Купфера и повышенной миграции моноцитов, дендритных клеток, нейтрофилов, активированных Т-лимфоцитов в ткани органа. Макрофаги, происходящие из моноцитов, по мере прогрессирования НАСГ постепенно начинают преобладать над пулом резидентных макрофагов. Риск развития НАСГ и фиброза у пациентов с НАЖБП повышается с увеличением соотношения нейтрофилов/лимфоцитов в печени. Увеличение количества Th17 и снижение — Treg-клеток могут способствовать усилению стеатоза печени и развитию воспаления при НАЖБП, а также ускорять переход от простого стеатоза к стеатогепатиту и фиброзу. Представлены сведения об участии некодирующих РНК в регуляции баланса иммунных клеток при НАЖБП, что позволяет также рассматривать их как дополнительные, наряду с клеточными, маркёры прогрессирования данного заболевания.

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