DCs-based therapies: potential strategies in severe SARS-CoV-2 infection.

Pneumonia caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is spreading globally. There have been strenuous efforts to reveal the mechanisms that the host defends itself against invasion by this virus. The immune system could play a crucial role in virus infection. Dendritic cell as sentinel of the immune system plays an irreplaceable role. Dendritic cells-based therapeutic approach may be a potential strategy for SARS-CoV-2 infection. In this review, the characteristics of coronavirus are described briefly. We focus on the essential functions of dendritic cell in severe SARS-CoV-2 infection. Basis of treatment based dendritic cells to combat coronavirus infections is summarized. Finally, we propose that the combination of DCs based vaccine and other therapy is worth further study.

MUC16 affects the biological functions of ovarian cancer cells and induces an antitumor immune response by activating dendritic cells.

BACKGROUND: Ovarian cancer is the 5th most common lethal gynecological malignancy with a 5-year survival rate of about 47% and a localized stage diagnosis of 15%, leading to about 125,000 global deaths each year. Therefore, it is urgent to explore novel and effective strategies for radical cure. METHODS: Short hairpin RNA targeting the Mucin16 (MUC16) gene was used to establish MUC16 knockdown in ovarian cancer cells. RT-PCR was performed to quantify the expression of MUC16 mRNA, and western blotting was performed to detect the expression of MUC16 and epithelial-mesenchymal transition-related proteins. Cell counting kit 8 (CCK8) wound healing and transwell assays were performed to assess cell proliferation and cell invasion. Flow cytometry was used to detect CD80-, CD83-, and CD86-expressing dendritic cells (DCs) and cytotoxic T lymphocytes (CTLs) activated by MUC16-pulsed DCs. RESULTS: In this study, we identified MUC16 as a novel target antigen for immunotherapy against ovarian cancer, which was significantly up regulated in ovarian cancer cells and high-grade ovarian serous adenocarcinoma tissues. MUC16 knockdown in Ovcar3 cells using short hairpin RNA targeting the MUC16 gene suppressed the proliferation of migration, invasion, epithelial-mesenchymal transition (EMT), and PI3K/Akt signaling pathway in Ovcar3 cells markedly. MUC16 significantly up-regulated CD80, CD83, and CD86 (mature makers) expression in DCs and T-cell transformation into CD8+ T-cells detected by Flow cytometry. CONCLUSIONS: For malignant ovarian cancer, MUC16 overexpression promoted cell proliferation, migration, and invasion via the PI3K/AKT signaling pathway. MUC16 pulsing mediated DC maturation and activated CTL response in vitro. Our study offers promising DC-based immunotherapy of considerable clinical value for patients with ovarian cancer.