New research suggests that dendritic cells produce and release CTLA-4, which typically inhibits anticancer responses.

Cancer immunotherapy strategies have made it increasingly evident that the immune system plays an integral role in managing and destroying cancer. Nevertheless, many mechanisms of immune suppression exist that may inhibit antitumour immunity. Recently, strategies that implement antibodies directed against negative immunologic regulators have demonstrated significant success. Cytotoxic T-lymphocyte-associate protein-4 (CTLA-4) was the first immunologic checkpoint to be clinically targeted, by the cancer immunotherapeutic ipilimumab, an FDA-approved drug to treat melanoma. After T-cell activation, CTLA-4 is upregulated on the cell surface where it functions to downregulate T cell function. Ipilimumab binds to CTLA-4 on T cells, which blocks the inhibitory signals and enhances anti-cancer immune responses.

In March 2016, Mark J Osborn et al published in Molecular Therapy a major article for genome editing (doi:10.1038/mt.2015.197), about knock-out of CD3 in human T-cells. The goal is to improve T-cell-based immunotherapies to fight tumours using engineered allogenic T-cells from healthy donors. It is a very good example of how CRISPR-CAS9 can help medecine. And even if you are not very comfortable with CAR T-cells and the treatments of malignancies, I would recommend you read it and especially take a look at figure 2. Indeed, dear friends of genome editing, the authors made a clear and fair comparison of several KO strategies, covering all the main options. Thus, it is not only a major step for anti-tumour treatments but it is also an excellent overview that reveals the best approaches. So, before reading this post any further, you might like to read the article mentioned above.