In the past year, from gene editing to eye tissue repair, we have witnessed a series of breakthroughs in the life sciences. The following are some of the exciting research reports in 2016:
Gene therapy: more precise
Accurate genome editing will allow us to treat a range of refractory and resistant diseases. Research from Harvard Medical School researchers (Nature 528, 490-495, 2016) brings us closer to highly specific nucleases One step:
The Cas9 protein of Streptococcus pyogenes can be edited together with sgRNAs, and sgRNAs can be paired with the target to direct nuclease binding to DNA, but it is not specific and therefore may cleave DNA sequences similar to the target sequence, resulting in Off-target effect. In this study, the researchers believe that non-specific cleavage may be due to the tight binding of nucleases to non-specific DNA sequences, so they synthesized a mutant nuclease that binds weakly to non-specific sequences in human cell experiments. They found that this nuclease can cleave more than 85% of the target sequence, but no non-specific cleavage is detected. This will allow future use of genetic editing for safer treatment, while also providing researchers with a strategy to optimize nucleases.
Gene therapy: a logical biological agent?
Some T cells in clinical trials have shown great potential, such as editing the endogenous receptors of T cells by genetic engineering or adding exogenous chimeric antigen receptors (CARs) to recognize antigens on the surface of cancer cells. However, since most of these antigens are also expressed in normal cells, this therapy often has serious side effects.
This year, Wendell Lim Laboratories reported a possible approach to improve CAR treatment, which relies on an evolutionarily conserved signaling pathway in which the Notch receptor controls gene transcription along with extracellular signals. Thereby controlling cell behavior. Using this feature, the researchers established a new regulatory mechanism: T cells first recognize an antigen of cancer cells through a synthetic Notch receptor (SynNotch) to activate CARs specific for another tumor antigen. Transcriptional translation (Cell 164, 780-791, 2016; Cell 164, 770-779, 2016). This combination can limit T cell killing of cells that express only these two antigens. This approach therefore improves selectivity and better control to reduce side effects during treatment. In tumor-bearing mice, SynNotch T cells specifically cleared cells that simultaneously expressed both antigens, but had no effect on cells expressing only one antigen. In a subsequent article in the same subject group, they showed that SynNotch T cells can differentiate into various effector cells required or selectively produce cytotoxic molecules, antibodies, cytokines and adjuvants, while these reactions only need to be synthesized. It can be controlled, independent of the endogenous T cell signaling pathway.
In fact, SynNotch T cells can be used to combat viral infection, hyperactivation, or other dysfunctional cells, which greatly broadens its field of application, but requires optimization to translate it into clinical applications.
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