LIMFOTSITLARARO O‘ZARO TA’SIRNING ANTAGONISTIK MEXANIZMLARI IMMUNITET MUVAOZANATINING MOLEKULYAR ASOSLARI
Abstract
Immunitet tizimining muvozanati va samaradorligi turli limfotsit subpopulyatsiyalari o‘rtasidagi murakkab va dinamik o‘zaro ta’sirlar natijasida shakllanadi. Ushbu maqolaning asosiy diqqat markazida limfotsitlarning bir-biriga antagonistik ta’sir ko‘rsatadigan, ya’ni bir guruhning boshqa guruhning faollashuvi, differentsiatsiyasi yoki efektor funksiyasini bevosita yoki bilvosita bostirishga qaratilgan mexanizmlari turadi. Bu jarayonlar immunitet javobini o‘z vaqtida to‘xtatish, o‘ta faollikdan himoya qilish va immunologik tolerantlikni saqlash uchun muhim ahamiyatga ega. Maqolada, birinchi navbatda, T-limfotsitlar o‘zaro antagonistik munosabatlari, xususan, regulyator T-limfotsitlar (Treg) ning effektor T-limfotsitlar (Teff), shu jumladan Th1, Th2 va Th17 xujayralari faolligini qanday boshqarishi chuqur tahsil qilinadi. Treg xujayralarining sitokinlar orqali (masalan, IL-10, TGF-β chiqarishi), metabolik raqobat (masalan, IL-2 ning yuqori affinitetli retseptorlari orqali ushlab qolinishi) va bevosita sitotoksiklik (granzim/perforin yo‘li) kabi turli usullar bilan immunosupressiv ta’siri ko‘rsatilgan [1]. Ikkinchi tomondan, effektor subpopulyatsiyalar o‘rtasidagi o‘zaro inhibitiv ta’sirlar, masalan, Th1 javobining IFN-γ orqali Th17 differentsiatsiyasini, yoki Th2 javobining IL-4 orqali Th1 faollashuvini suprimasi muhokama qilinadi [2]. Shuningdek, B-limfotsitlar va ularning ishlab chiqargan antitanachalari T-hujayrali faollikni modulyatsiya qilishi, shu jumladan idiotipik tarmoqlar orqali immunosupressiv ta’sir ko‘rsatishi ham antagonistik mexanizmlar doirasida ko‘rib chiqiladi [3]. Yaqin yillarda o‘rganilgan yangi mexanizmlar, jumladan, ekzozomlar orqali inhibitiv mikroRNAlarning uzatilishi, chek nuqtasi (checkpoint) molekulalari (masalan, CTLA-4, PD-1) faolligi va turli metabolik yo‘llarning (masalan, triptofan metabolizmi) roli tahsil etilgan [4, 5]. Ushbu mexanizmlarning buzilishi o‘ta faol yoki, aksincha, yetarli darajada bo‘lmagan immun javobga olib kelishi mumkin, bu esa avtoimmun kasalliklar, surunkali yallig‘lanish, allergik reaksiyalar va immunitet tanqisligi bilan bog‘liq kasalliklarning patogenezida hal qiluvchi ahamiyatga ega. Ushbu tadqiqot limfotsitlararo antagonistik o‘zaro ta’sirlarni tushunish orqali yangi immunomodulyator terapiyalar, masalan, Treg funktsiyasini kuchaytirish yoki maqsadli chek nuqtasi inhibitirlarini ishlab chiqish uchun ilmiy asos yaratishga qaratilgan [6].
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