СЕМІЗДІККЕ БАЙЛАНЫСТЫ БАУЫР ҚАТЕРЛІ ІСІГІНДЕГІ ИММУНДЫҚ ЖАСУШАЛАРДЫҢ РӨЛІ

Кіріспе. Семіздік гепатоцеллюлярлы карциноманың  тәуелсіз қауіп факторы ретінде танылған, ол дүниежүзі бойынша қатерлі ісіктен болатын өлімнің үшінші жетекші себебі болып табылады. Қазақстанда ересек халықтың 20%-дан астамы семіздікпен ауырады және бауыр қатерлі ісігінің таралуы тұрақты өсу үрдісін көрсетеді, бұл аталған байланысқа жедел денсаулық сақтау маңызын береді. Семіздік пен гепатоцеллюлярлы карцинома арасындағы эпидемиологиялық байланыс жақсы дәлелденгеніне қарамастан, семіздіктің ісікке қарсы иммунитетті бұзу және бауырдың микроортасын қалыптастыру механизмдері толық зерттелмеген. Осы шолу созылмалы метаболикалық стресс жағдайында алкогольсіз майлы бауыр ауруыдан ГЦК-ға дейінгі үдерісте туа біткен және адаптивті иммундық жасушалардың қалай өзгеретінін талдайды.

Мақсаты: Семіздік жағдайында бауыр қатерлі ісігінің дамуындағы иммундық және қабыну механизмдерінің рөліне қатысты қазіргі ғылыми деректерді талдау, сондай-ақ метаболикалық бұзылыстардың ісікке қарсы иммундық жауапқа және бауырдың микроортасына әсері туралы мәліметтерді жүйелеу.

Материалдар мен әдістер: Жүйелі әдебиетті іздеуі PubMed, Google Scholar, Scopus және Web of Science халықаралық деректер қорларында 2000 жылдан 2026 жылға дейінгі кезеңдегі халықаралық және отандық басылымдарды қамти отырып жүргізілді.

Нәтижелер мен талқылау: Семіздікпен байланысты гепатоцеллюлярлы карцинома висцеральды май ұлпасы қатерлі өзгеріс пайда болғанға дейін иммуносупрессивті микроортаны қалыптастыратын прогрессивті иммунометаболикалық каскад арқылы дамиды - миелоидтан алынған супрессорлық жасушалар (MDSC) кеңеюі, NK-жасушалардың дисфункциясы және CD8⁺ Т-жасушалардың сарқылуы арқылы. Реттеуші Т-жасушалар (Treg) семіз май ұлпасында азаяды, бірақ ГЦК-да жиналады; алкогольсіз стеатогепатит кезіндегі NK-жасушалардың белсенділігі ісіктен қорғаудың орнына гепатоциттерге зақым келтіреді. Патологиялық нәтижені жасушалардың саны емес, олардың функционалдық поляризация күйі анықтайды.

Қорытынды: Семіздік май ұлпасының созылмалы қабынуы, инсулинрезистенттілік және ісік микроортасының метаболикалық қайта бағдарламалануы арқылы гепатоцеллюлярлы карцинома дамуын жеделдетеді, цитотоксикалық CD8⁺ Т-жасушалары мен NK-жасушаларын сарқып, иммуносупрессивті Treg және MDSC-ның кеңеюіне ықпал етеді. Бауыр қатерлі ісігінің прогрессиясы тек вирустық немесе уытты факторлармен ғана емес, сонымен қатар семіздік туындататын иммундық теңгерімсіздікпен де байланысты, онда жүйелі метаболикалық стресс ісіктің иммундық бақылаудан жасырынуының негізгі факторына айналады.

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