Cytotoxic T-lymphocytes are important effectors in the clearance of virally infected and cancerous cells, and defects in their function give rise to many pathologies.

Cytotoxic T lymphocytes (CTLs) are key effectors of the adaptive immune system that recognize and eliminate virally infected and cancerous cells. In naive CD8⁺ T cells, T-cell receptor (TCR) engagement drives a number of transcriptional, translational and proliferation changes over the course of hours and days leading to differentiation into CTLs. To gain a better insight into this mechanism, we compared the transcriptional profiles of naive CD8⁺ T cells to those of activated CTLs. To find new regulators of CTL function, we performed a selective clustered regularly interspaced short palindromic repeats (CRISPR) screen on upregulated genes and identified nuclear factor IL-3 (NFIL3) as a potential regulator of cytotoxicity. Although NFIL3 has established roles in several immune cells including natural killer, Treg, dendritic and CD4⁺ T cells, its function in CD8⁺ CTLs is less well understood. Using CRISPR/Cas9 editing, we found that removing NFIL3 in CTLs resulted in a marked decrease in cytotoxicity. We found that in CTLs lacking NFIL3 TCR-induced extracellular signal-regulated kinase phosphorylation, immune synapse formation and granule release were all intact while cytotoxicity was functionally impaired in vitro. Strikingly, NFIL3 controls the production of cytolytic proteins as well as effector cytokines. Thus, NFIL3 plays a cell intrinsic role in modulating cytolytic mechanisms in CTLs.

CD8⁺ cytotoxic T lymphocytes (CTLs) are key effectors of the adaptive immune response that precisely recognize and eliminate virally infected and cancerous cells. In naive CD8⁺ T cells, T-cell receptor (TCR) engagement induces a number of transcriptional, translational and proliferation changes over the course of hours and days leading to differentiation into CTLs [1,2]. TCR ligation of differentiated CTLs drives a rapid response and the formation of a transient area of plasma membrane specialized in signalling and polarized secretion, termed the immune synapse [3]. CTLs undergo rapid rearrangements in microtubule and actin cytoskeletons as the centrosome and microtubule network polarize towards the synapse and cortical actin is transiently depleted [4–7].

Because identical twins develop from a single fertilized egg, they have the same genome, the entire set of genetic material found in an organism. So, any differences between them, even in traits with a significant genetic component – say one develops heart disease and the other doesn’t – are due to their environments. This is known as epigenetics.

Genes in DNA are ‘expressed’ when they’re read and transcribed into RNA, which is then translated into proteins. It’s proteins that determine many of a cell’s characteristics and functions. Epigenetic changes can boost or silence the transcription of specific genes, ramping up or inhibiting associated protein production, but they don’t change the genome. These changes, which are reversible, can affect a person for their entire life and mediate a lifelong dialogue between genes and the environment.

Researchers from Australia and a private biotechnology firm in the US have successfully demonstrated the use of high-frequency radio waves to temporarily open up bacterial cell walls to introduce new genetic material into them.

High frequency radio waves are a far efficient method to add DNA to bacterial cells than conventional approaches such as heat shock.

Researchers at the University of Alberta have uncovered what they say has been the missing puzzle piece ever since the genetic code was first cracked.

The code is the universal set of rules that allow living organisms to follow genetic instructions found in DNA and RNA to build proteins. In new research, published in BMC Biology, the U of A team describes a unifying code that guides the binding of those proteins with lipids to form membranes—the wrapper around all cells and cell components.

“Sixty years ago, scientists started to work on how genes encode proteins, but that’s not the end of the story,” says biochemistry professor Michael Overduin, executive director of the National High Field Nuclear Magnetic Resonance Center. “Along with DNA, RNA and proteins, living cells require membranes. Without the membrane, it’s like you’ve got a house with no walls.”

One of the immune system’s primary roles is to detect and kill cells that have acquired cancerous mutations. However, some early-stage cancer cells manage to evade this surveillance and develop into more advanced tumors.

A new study from MIT and Dana-Farber Cancer Institute has identified one strategy that helps these precancerous cells avoid immune detection. The researchers found that early in colon cancer development, cells that turn on a gene called SOX17 can become essentially invisible to the immune system.

If scientists could find a way to block SOX17 function or the pathway that it activates, this may offer a new way to treat early-stage cancers before they grow into larger tumors, the researchers say.