TUBERKULYOZ KASALLIGIDA MYCOBACTERIUM TUBERCULOSIS-NING IMMUN EVASIYA MEXANIZMLARI VA ZAMONAVIY TERAPEVTIK MAQSADLAR
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Mycobacterium tuberculosis, immun evasiya, fagosoma, MDR-TB, bedaquiline, granuloma dinamikasi.Abstrak
Tuberkulyoz patogenezida Mycobacterium tuberculosis-ning makrofaglar ichida saqlanib qolish mexanizmlari hali to'liq o'rganilmagan. Ushbu tezisda fagosoma-lizosom qo'shilishini bloklash, reaktiv kislorod turlarini neytrallash va T-limfotsit apoptozini modulyatsiya qilish orqali sodir bo'luvchi immun evasiya yo'llari tahlil qilinadi. Bedaquiline va delamanid preparatlarining ATP-sintaza va metanogenez yo'llariga selektiv ta'siri asosida MDR-TB davolashda yangi terapevtik oyna mavjudligi ko'rsatiladi.
Iqtiboslar
Vergne I. et al. Mechanism of phagolysosome biogenesis block by viable M. tuberculosis. J Exp Med. 2004;201(2):263–274.
Nathan C, Shiloh MU. Reactive oxygen and nitrogen intermediates in the relationship between mammalian hosts and microbial pathogens. PNAS. 2000;97(16):8841–8848.
Divangahi M. et al. Mycobacterium tuberculosis evades macrophage defenses by inhibiting plasma membrane repair. Nat Immunol. 2009;10(8):899–906.
Ramakrishnan L. Revisiting the role of the granuloma in tuberculosis. Nature Rev Immunol. 2012;12(5):352–366.
Diacon AH. et al. The diarylquinoline TMC207 for multidrug-resistant tuberculosis. N Engl J Med. 2009;360(23):2397–2405.
Gler MT. et al. Delamanid for multidrug-resistant pulmonary tuberculosis. N Engl J Med. 2012;366(23):2151–2160.
WHO. Global Tuberculosis Report 2023. Geneva: WHO Press; 2023.
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