PHENOTYPE AND FUNCTIONS OF DENDRITIC CELLS IN PATIENTS WITH CHRONIC VIRAL HEPATITIS
https://doi.org/10.15789/1563-0625-2009-2-3-191-196
Abstract
Abstract. Phenotypic and functional features of IFNα-induced dendritic cells (DCs) were studied in patients with chronic viral hepatitis B and C (HBV and HCV), and in cases with hepatitis-related liver cirrhosis (LC). It was shown that DCs are characterized by delayed differentiation/maturation which was more pronounced in HCV patients, as well as in all patients with LC, regardless of virus type. DCs from HBV patients were characterized by increased IFNγ secretion. Transformation of HBV-infection to LC is accompanied by a moderate decrease in IFNγ production, combined with a significantly increased IL-10 secretion. Irrespectively of fibrosis severity, the IFNα-induced DCs of HCV patients displayed active IL-10 synthesis. Moreover, ability of DCs to secrete IFNγ was significantly decreased only in cases of fibrosis-complicated HCV-infection. With respect to TNFα and IL-4 production levels, DCs of the patients were compatibe to normal donor cells, independently on the type of virus, or fibrosis severity. DCs from HBV- and HCV-patients were characterized by intact allostimulatory and Th1/Th2-stimulatory activities in MLC. At the same time, IFNα-induced DCs exhibited suppression of allostimulatory and increase in Th2-polarizing activity upon LC development, both in HBV and HCV patients.
About the Authors
O. Yu. LeplinaRussian Federation
M. A. Tikhonova
Russian Federation
A. E. Borisova
Russian Federation
N. M. Starostina
Russian Federation
A. A. Ostanin
Russian Federation
E. R. Chernykh
Russian Federation
V. A. Kozlov
Russian Federation
References
1. Arima S., Akbar S.M., Michitaka K. et al. Impaired function of antigen-presenting dendritic cells in patients with chronic hepatitis B: localization of HBV DNA and HBV RNA in blood DC by in situ hybridization // Int. J. Mol. Med. – 2003. – Vol. 11. – P. 169-174.
2. Auffermann-Gretzinger S., Keeffe E.B., Shoshana L.S. Impaired dendritic cell maturation in patients with chronic, but not resolved, hepatitis C virus infection // Blood. – 2001. – Vol. 97, N. 10. P. 3171-3176.
3. Banchereau J., Steinmann R.M. Dendritic cells and control of immunity // Nature. – 1998. – Vol. 392. – P. 245-252.
4. Duan X.Z., Wang M., Li H.W., Liu J.C., Wang F.S. Decreased numbers and impaired function of circulating dendritic cell subsets in patients with chronic hepatitis B infection // J. Gastroenterol. Hepatol. – 2005. – Vol. 20. – P. 234-242.
5. Fowler N.L., Torresi J., Jackson D.C., Lorena E.B., Gowans E.J. Immune responses in hepatitis C virus infection: The role of dendritic cells // Immunol. Cell Biology. – 2003. – Vol. 81. – P. 63 - 66.
6. Kanto T., Takenara T. Immunopathogenesis of type C hepatitis: dendritic cell in HCV infection // J. Gastroenterol. Hepatol. – 2004. – Vol. 19. – N 7. – P. 84-87.
7. Kakumu S, Ito S, Ishikawa T, et al. Decreased function of peripheral blood dendritic cells in patients with hepatocellular carcinoma with hepatitis B and C virus infection // J. Gastronterol Hepatol. – 2000. – Vol. 15. – P. 431-436.
8. Murakami H., Akbar S.M.F, Matsui H., Horike N., Onji M. Decreased interferon-alpha production and impaired T helper 1 polarization by dendritic cells from patients with chronic hepatitis C // Clin. Exp. Immunol. – 2004. – Vol. 137. – P. 559-565.
9. Parlato S., Santini S., Lapenta C., Di Pucchio T., Logozzi M., Spada M., Giammarioly A., Malorni W., Fais S., Bellardelli F. Expression of CCR-7, MIP-3b, and Th1 chemokines in type I IFN-induced monocyte-derived dendritic cells – importance for the rapid acquisition of potent migratory and functional activities // Blood. – 2001. – Vol. 98. – P. 3022-3029.
10. Santini S., Lapenta C., Logozzi M., Parlato S., Spada M., Di Pucchio T., Bellardelli F. Type I Interferon as a powerful adjuvant for monocytederived dendritic cells development and activity in vitro and in HU-PBL-SCID mice // J. Exp. Med. – 2000. – Vol. 191. – P. 1777-1788.
11. Santini S., Pucchini T., Lapenta C., et al. A new type 1 IFN-mediated pathway for the rapid differentiation of monocytes into highly active dendritic cells // Stem cells. – 2003. – Vol. 21. – P. 357-362.
12. Tavakoli S., Schwerin W., Rohwer A., Hoffmann S., Weyer S., Weth R., Meisel H., Diepolder H., Geissler M., Galle P.R., Bocher H.F. Phenotype and function of monocyte derived dendritic cells in chronic hepatitis B virus infection // J. General Virology. – 2004. – Vol. 85. – P. 2829-2836.
13. Thurner B., Roder C., Dieckmann D., Heuer M., Kruse M., Glaser A., Keikavoussi P., Kampgen E., Bender A., Schuler G. Generation of large numbers of fully mature and stable dendritic cells from leukapheresis products for clinical applications // J. Immunol. Meth. – 1999. – Vol. 223. – P. 1-15.
14. Tsubouchi E., Akbar S.M.F., Murakami H., Horiike N., Onji M. Isolation and functional analysis of circulating dendritic cells from hepatitis C virus (HCV) RNA-positive and HCV RNA-negative patients with chronic hepatitis C: role of antiviral therapy // Clin. Exp. Immunol. – 2004. – Vol. 137, N 2. – P. 417-423.
15. Ulsenheimer A., Gerlach J.T., Jung M.C., et al. Plasmacytoid dendritic cells in acute and chronic hepatitis C virus infection // Hepatology. – 2005. – Vol. 41, N 3. – P. 643-651.
16. Wang F-S., Xing L-X., Liu M-X., Zhu C-L., Liu H-G., Wang H-F., Lei Z-Y. Dysfunction of peripheral blood dendritic cells from patients with chronic hepatitis B virus infection // Wold J. Gastroenterol. – 2001. – Vol. 7. – P. 537-541.
17. Zheng B.J., Zhou J., Qu D., Siu K.L., Lam T.W., Lo H.Y., Lee S.S., Wen Y.M. Selective functional deficit in dendritic cell – T cell interaction is a crucial mechanism in chronic hepatitis B virus infection // J. Viral Hepatitis. – 2004. – Vol. 11. – P. 217-224.
Review
For citations:
Leplina O.Yu., Tikhonova M.A., Borisova A.E., Starostina N.M., Ostanin A.A., Chernykh E.R., Kozlov V.A. PHENOTYPE AND FUNCTIONS OF DENDRITIC CELLS IN PATIENTS WITH CHRONIC VIRAL HEPATITIS. Medical Immunology (Russia). 2009;11(2-3):191-196. (In Russ.) https://doi.org/10.15789/1563-0625-2009-2-3-191-196