Decreased IRF7 Expression Contributes to Deficient IFN-ÃÂ± Production of Plasmacytoid Dendritic Cells in Chronic HIV-1 Infected Men who have Sex with Men
Wenqing Geng, Sha Li, Xuejie Fan, Fang Gao, Hualu Cui, Hong Sun, Zining Zhang, Yongjun Jiang and Hong Shang*
Department of Laboratory Medicine, First Hospital of China Medical University, Shenyang, China
- *Corresponding Author:
- Hong Shang, Director
Key Laboratory of AIDS Immunology of Ministry of Health
Department of Laboratory Medicine
First Hospital of China Medical University
Address: No. 155, Nanjingbei Street
Heping District, Shenyang
Liaoning province, 110001, China
E-mail: [email protected] hotmail.com
Received date: December 01, 2015; Accepted date: February 22, 2016; Published date: February 27, 2016
Citation: Geng W, Li S, Fan X, Gao F, Cui H, et al. (2016) Decreased IRF7 Expression Contributes to Deficient IFN-α Production of Plasmacytoid Dendritic Cells in Chronic HIV-1 Infected Men who have Sex with Men. J AIDS Clin Res 7:548. doi:10.4172/2155-6113.1000548
Copyright: © 2016 Geng W, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Deficient interferon (IFN)-α production of plasmacytoid DCs (pDCs) from HIV-1-infected individuals in response to virus or toll-like receptor (TLR) stimulation has been reported. pDCs express TLR7 and TLR9, but whether and how the TLR pathway contributes to the deficiency has not been well addressed.
Methods: Twenty-six subjects with HIV-1 infection were recruited from a chronic HIV-1 infection (CHI) cohort of men who have sex with men (MSM) and 15 HIV-1 negative healthy MSM were used as normal controls (NCs). Maturation markers (CD80, CD86, CD83, CD40, CCR7), TLR7 and TLR9, nuclear factor κB (NF-κB) and interferon regulatory factor 7 (IRF7) expression were detected using surface and intracellular multicolor flow cytometry. Intracellular IFN-α production of pDCs was measured in response to R848 (TLR7 agonist) and ODN2216 (TLR9 agonist), respectively.
Results: IFN-α production of pDCs with treatment of R848, but not ODN2216, from MSM with CHI was significantly lower than that of NCs. There was no significant difference in maturation marker expression between MSM with CHI and NCs. The expression of TLR7 and TLR9 on pDCs of MSM with CHI was significantly up-regulated. The expression of IRF7, a downstream signaling protein in the TLR7/9 signaling pathway, was significantly down-regulated as compared with that of NCs. NF-κB expression of pDCs of MSM with CHI were similar to that of NCs.
Conclusions: These results indicated that decreased IRF7 expression might contribute to deficient IFN-α production in MSM with CHI, suggesting efforts to increase the expression of IRF7 might resume the function of pDCs in individuals with CHI.