Development of NK cell expansion methods using feeder cells from human myelogenous leukemia cell line

BACKGROUND: Natural killer (NK) cells constantly survey surrounding tissues and remove newly generated cancer cells, independent of cancer antigen recognition. Although there have been a number of attempts to apply NK cells for cancer therapy, clinical application has been somewhat limited because of the difficulty in preparing a sufficient number of NK cells. Therefore, ex vivo NK cell expansion is one of the important steps for developing NK cell therapeutics. METHODS: CD3+ depleted lymphocytes were cocultured with IL-2 and with feeder cells (peripheral blood mononuclear cells [PBMCs], K562, and Jurkat) for 15 days. Expanded NK cells were tested for cytotoxicity against cancer cell lines. RESULTS: We compared feeder activities of three different cells-PBMC, K562, and Jurkat. K562 expanded NK cells by almost 20 fold and also showed powerful cytotoxic activity against cancer cells. K562-NK cells remarkably expressed the NK cell activation receptors, NKG2D, and DNAM-1. K562-NK cells exhibited more than two-fold production of cytotoxic granules compared with Jurkat-NK cells, producing more perforin and granzyme B than naive NK cells. CONCLUSION: Our findings suggest that K562 are more efficient feeder cells than Jurkat or PBMCs. K562 feeder cells expanded NK cells by almost 20 fold and showed powerful cytotoxic activity against cancer cells. We herein propose an intriguing approach for a design of NK cell expansion.

Recent advances in the anti-HCV mechanisms of interferon

Interferon (IFN) in combination with ribavirin has been the standard of care (SOC) for chronic hepatitis C for the past few decades. Although the current SOC lacks the desired efficacy, and 4 new direct-acting antiviral agents have been recently approved, interferons are still likely to remain the cornerstone of therapy for some time. Moreover, as an important cytokine system of innate immunity, host interferon signaling provides a powerful antiviral response. Nevertheless, the mechanisms by which HCV infection controls interferon production, and how interferons, in turn, trigger anti-HCV activities as well as control the outcome of HCV infection remain to be clarified. In this report, we review current progress in understanding the mechanisms of IFN against HCV, and also summarize the knowledge of induction of interferon signaling by HCV infection.

Expression of DNAM-1 on T cells subsets from patients with systemic lupus erythematosus / 中国免疫学杂志

Objective:To investigate functional of DNAM 1 antigen in T cell subsets activation process from patients with SLE and determine whether they are correlated with the pathogenesis of SLE.Methods:The peripheral blood monouclear cells from 31 SLE and 30 healthy volunteers were stimulated with PHA.Those cells were quantified using flow cytometric analysis with three colour immunofluorescent staining method.The levels of anti dsDNA,complement C 3 and C 4 were measured as well as.Results:The percentages of DNAM 1 positive from SLE on CD + 4 and CD + 8 T cells were increased,compared with that of the controls (P0.05).The DNAM 1 expression on CD + 8 cells from SLE showed relatively high positive correlation with SLEDAI and anti dsDNA antibody and that on CD + 8 T cells have negative correlation with C 3 and C 4 complement(P0.05).Conclusion:There are some abnormal activated T cell subsets in SLE.The expression of DNAM 1 on CD + 4?CD + 8 T cells with active SLE are increased.That on CD + 8 cells are correlated to SLEDAI?anti dsDNA antibody?C 3 and C 4 complement and there is a clinical correlation with it's levels.So DNAM 1 may play an important roles in the mechanisms of immune activation and immunopathology in SLE.