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P156 Study on the effect of slanDC-mediated ADCC in HIV-1-infected patients
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  1. Qian Jiang1,
  2. H Sun2,
  3. Hualu Cui1,
  4. Wenqing Geng1,
  5. Hong Shang1
  1. 1The First Affiliated Hospital, China Medical University, Shenyang, China
  2. 2AIDS Institute, China Medical University, Shenyang, China

Abstract

Background Antibody-dependent cell-mediated cytotoxicity (ADCC) mediated by natural killer (NK) cells plays a critical role in HIV-1 infection. As a novel subset of dendritic cells (DCs), 6-sulfo LacNAc-expressing DCs (slanDCs) also express CD16. However, the levels of slanDC-mediated ADCC during HIV-1 infection are not well addressed.

Methods Forty-five HIV-1-infected subjects were enrolled and 19 HIV-1 negative individuals were used as healthy controls (HCs). The complex of gp120 and anti-gp120 was used to stimulate peripheral blood mononuclear cells (PBMCs) and the level of TNF-alpha secreted by slanDCs was detected using intercellular staining of flow cytometer.

Results The counts of slanDCs in HIV-1-infected and treatment naïve patients were significantly lower than those of HCs and those receiving anti-retrovirus therapy (ART) (P=0.0331, P<0.0001). The number of slanDCs in HIV-1-infected patients with ART was significantly higher than those who did not receive ART, indicating that ART could help HIV-1-infected individuals to recover the number of slanDCs. The level of slanDC-medated ADCC evaluated as the level of TNF-alpha production by slanDCs stimulated by the complex of gp120-anti-gp120, was significantly lower in HIV-1-infected subjects as compared with HCs and those receiving ART (P=0.0011, P=0.0002). The expression of CD16 (MFI) by slanDCs from HIV-1-infected patients receiving ART was significantly higher than that from HIV-1-infected untreated and HCs (P=0.0014, P=0.0003), and the expression of CD16 (MFI) in slanDC was positively correlated with the ADCC effect (P<0.0001).

Conclusion The slanDC-medated ADCC existed in HIV-1-infected patients and the level could be enhanced by ART, suggesting an alternative pathway involved in ADCC in HIV-1 infection.

Disclosure No significant relationships.

  • HIV

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