【摘要】 白細胞介素-28B(IL-28B)是一種重要的細胞因子,也被稱之為干擾素-λ3 (IFN-λ3),其作用機制類似于IFN-α,通過誘導受體異二聚體化,活化JAK-STAT信號通路,進而發(fā)揮抗病毒、免疫調(diào)節(jié)等生物學作用。最近國外研究團隊相繼發(fā)現(xiàn)IL-28B基因附近的單核苷酸多態(tài)性與干擾素聯(lián)合利巴韋林治療慢性丙型病毒性肝炎的療效密切相關(guān)。這有助于通過宿主基因水平更準確的預測患者治療效果,并有可能在將來提供一種更有效的治療方案。
引用本文: 徐輝,雷學忠. 白細胞介素-28B附近基因多態(tài)性與慢性丙型肝炎的抗病毒治療相關(guān)性的研究進展. 華西醫(yī)學, 2011, 26(1): 139-141. doi: 復制
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13. | Marcello T, Grakoui A, Barba-spaeth G, et al. Interferons alpha and lambda inhibit hepatitis C virus replication with distinct signal transduction and gene regulation kinetics[J]. Gastroenterology, 2006, 131(6): 1887-1898. |
14. | Suppiah V, Moldowan M, Ahlenstiel G, et al. IL28B is associated with response to chronic hepatitis C interferon-alpha and ribavirin therapy[J]. Nat Genet, 2009, 41(10): 1100-1174. |
15. | Tanaka Y, Nishida N, Sugiyama M, et al. Genome-wide association of IL28B with response to pegylated interferon-alpha and ribavirin therapy for chronic hepatitis C[J]. Na Genet, 2009, 41(10): 1105-1181. |
- 1. Ghany MG, Strader DB, Thomas DL, et al. Diagnosis, management, and treatment of hepatitis C: an update[J]. Hepatology, 2009, 49(4): 1335-1374.
- 2. Amin J, Dore GJ, O’connell DL, et al. Cancer incidence in people with hepatitis B or C infection: a large community-based linkage study[J]. J Hepatol, 2006, 45(2): 197-203.
- 3. Zeuzem S, Berg T, Moeller B, et al. Expert opinion on the treatment of patients with chronic hepatitis C[J]. J Viral Hepatitis, 2009, 16(2): 75-90.
- 4. Hadziyannis SJ, Sette H, Morgan TR, et al. Peginterferon-alpha 2a and ribavirin combination therapy in chronic hepatitis C - A randomized study of treatment duration and ribavirin dose[J]. Ann Intern Med, 2004, 140(5): 346-355.
- 5. Liu CH, Liu CJ, Lin CL, et al. Pegylated interferon-alpha-2a plus ribavirin for treatment-naive Asian patients with hepatitis C virus genotype 1 infection: a multicenter, randomized controlled trial[J]. Clin Infect Dis, 2008, 47(10): 1260-1269.
- 6. Yan KK, Guirgis M, Dinh T, et al. Treatment responses in Asians and Caucasians with chronic hepatitis C infection[J]. World J Gastroenterol, 2008, 14(21): 3416-3420.
- 7. Sheppard P, Kindsvogel W, Xu WF, et al. IL-28, IL-29 and their class II cytokine receptor IL-28R[J]. Nat Immunol, 2003, 4(1): 63-68.
- 8. Kotenko SV, Gallagher G, Baurin VV, et al. IFN-lambda s mediate antiviral protection through a distinct class II cytokine receptor complex[J]. Nat Immunol, 2003, 4(1): 69-77.
- 9. Ge DL, Fellay J, Thompson AJ, et al. Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance[J]. Nature, 2009, 461(7262): 399-401.
- 10. Thomas DL, Thio CL, Martin MP, et al. Genetic variation in IL28B and spontaneous clearance of hepatitis C virus[J]. Nature, 2009, 461(7265): 798-801.
- 11. Robek MD, Boyd BS, Chisari FV. Lambda interferon inhibits hepatitis B and C virus replication[J]. J Virol, 2005, 79(6): 3851-3854.
- 12. Ank N, West H, Bartholdy C, et al. Lambda interferon (IFN-lambda), a type III IFN, is induced by viruses and IFNs and displays potent antiviral activity against select virus infections in vivo[J]. J Virol, 2006, 80(9): 4501-4509.
- 13. Marcello T, Grakoui A, Barba-spaeth G, et al. Interferons alpha and lambda inhibit hepatitis C virus replication with distinct signal transduction and gene regulation kinetics[J]. Gastroenterology, 2006, 131(6): 1887-1898.
- 14. Suppiah V, Moldowan M, Ahlenstiel G, et al. IL28B is associated with response to chronic hepatitis C interferon-alpha and ribavirin therapy[J]. Nat Genet, 2009, 41(10): 1100-1174.
- 15. Tanaka Y, Nishida N, Sugiyama M, et al. Genome-wide association of IL28B with response to pegylated interferon-alpha and ribavirin therapy for chronic hepatitis C[J]. Na Genet, 2009, 41(10): 1105-1181.