TIZIMLI SKLEROZDA OʻSISH OMILI-Β1NING OʻRNI
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Tizimli skleroz, transformatsion o'sish omili-b, mexanizm.Abstrak
Tizimli skleroz (SSc) noma'lum etiologiyali murakkab, ko'p organli autoimmun kasallikdir. Kasallikning namoyon bo'lishi uchta asosiy patologik xususiyatning o'zaro ta'siridan kelib chiqadi, shu jumladan antigenga xos immunitet tizimi va o'ziga xos bo'lmagan immunitet tizimining nosog'lomligi, natijada otoantikor ishlab chiqarish, mayda qon tomirlarining tomir endotelial faollashuvi va fibroblast disfunktsiyasi natijasida to'qima fibrozi. Kasallikning klinik ko'rinishining geterogenligini hisobga olgan holda, universal modellarning etishmasligi SSc uchun potentsial davolash usullarini etarli darajada sinovdan o'tkazishga to'sqinlik qildi. Qanday bo'lmasin, yaqinda o'tkazilgan tadqiqotlar kasallikning klinik ko'rinishiga hissa qo'shadigan turli xil molekulyar mexanizmlarning rolini aniqladi. Transformatsiya qiluvchi o'sish omili b (TGF-b) SScda patologik fibrogenezning regulyatori sifatida aniqlangan. Hujayra o'sishi, apoptoz, hujayra differentsiatsiyasi va hujayradan tashqari matritsa sintezi kabi turli jarayonlar makrofaglar va boshqa ko'plab hujayralar tomonidan chiqariladigan sitokin turi TGF-b tomonidan boshqariladi. Tizimli skleroz patologiyasida TGF-b yo'llarining muhim rolini tushunish davolash uchun potentsial yo'l va ushbu og'ir kasallikni yaxshiroq tushunish imkonini beradi
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