Katharina Buczek
First, the team created a model based on tumor cells. Then, they produced exhausted lymphocytes– which are similar to the T cells found in patient tumors. Afterward, the researchers analyzed various genes by individually inactivating them. This inactivation was accomplished using a gene editing process known as CRISPR/Cas9.
In doing so, the team successfully identified one gene– known as SNX9– that is responsible for regulating T cell exhaustion. They found that when the gene is inactivated, T cells remain functional– regardless of whether they are located near a tumor for a longer period of time.
In other words, the SNX9 gene seemingly increases short-term immune response– which can be very important in instances when each hour counts in the fight against diseases.
“In the case of our experiment, however, suppressing the SNX9 gene enabled finer adjustment of immune cell activity by reducing excessive stimulation signals. The T cells’ activity was, therefore, conserved over a longer period,” explained Marcel Trefny, the study’s lead author.
Finally, the study also revealed how instead of just dying after completing their jobs, the T cells more frequently developed into memory T cells.
According to Zippelius, this discovery of SNX9’s role may pave the way for more efficient immunotherapies in the future. In the meantime, though, clinical tests regarding the therapeutic application of this gene inactivation must be conducted to determine whether the absence of SNX9 leads to adverse effects.
To read the study’s complete findings, which have since been published in Nature Communications, visit the link here.
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