The response to TLR ligation of human CD16⁺CD14^− monocytes is weakly modulated as a consequence of persistent infection with the hepatitis C virus

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• 作者：Cheng Peng^a ; ^b ; ¹ ; Bi-Sheng Liu^a ; ¹ ; Robert J. de Knegt^a ; Harry L.A. Janssen^a ; André ; Boonstra^a ; ^{p.a.boonstra@erasmusmc.nl"" rel=""nofollow}
• 关键词：Monocyte subset ; TLR ; Viral infection ; Hepatitis C virus
• 刊名：Molecular Immunology
• 出版年：2011
• 出版时间：July 2011
• 年：2011
• 卷：48
• 期：12-13
• 页码：1505-1511
• 全文大小：523 K

文摘

Little is known about the frequency and function of CD16⁺CD14^− monocytes from chronic HCV patients. We observed that the absolute numbers and ratio of CD16⁺CD14^− to CD14⁺CD16^− monocytes were similar between chronic HCV patients and healthy individuals. Functionally, we found that CD16⁺CD14^− monocytes are more responsive to TLR8-ligation and only weakly responsive to LPS stimulation in producing TNF as compared to CD14⁺CD16^− monocytes. We found no overt impairment of the function of CD16⁺CD14^− monocytes from patients, except for an augmented induction of MIP-1β-producing CD16⁺CD14^− monocytes upon TLR4-ligation. However, the increased frequency of MIP-1β-producing CD16⁺CD14^− monocytes was not associated with viral load, ALT or fibrosis level. Our findings indicate that, different from other infectious diseases, the frequency and function of CD16⁺CD14^− monocytes are only minimally altered as a consequence of the persistent state of HCV infections, and our findings therefore do not suggest a role for CD16⁺CD14^− monocytes in HCV pathogenesis.