In order to rapidly and efficiently respond to new infections, the immune system evolved such that it stores a 'memory' of previous attack by pathogens. The specialized cells involved in this process are known as 'T memory cells'. The T memory cells are normally maintained at a low level that can be rapidly expanded if the pathogen is detected again. The maintenance of normal, low levels, or 'homeostasis', of T memory cells is dependent on a signalling factor, a so-called cytokine, known as 'IL- 15.
'Very little is known about the signalling pathways that actually control IL-15-dependent homeostasis,' explains LICR's Dr. H. Robson MacDonald, the senior author of the study. 'By analyzing genetically engineered mouse models with reduced c-myc, reduced IL-15 or absent IL-15, we discovered that it's actually c-myc, which is known primarily as an oncogene, that acts downstream of the IL-15 signaling pathway to regulate T memory cell homeostasis.'
According to Dr. MacDonald, the study is basic research that may have implications for therapies of the future. 'Understanding how immune memory works might allow us to improve therapeutic vaccines against, say, malaria or cancer. The unexpected finding is that this study is also a cautionary tale. Before we design new therapies that inactivate a gene product, which is an approach being considered for c-myc in cancer, we need to be very sure that we are not going to be also destroying a vital role in a normal process such as the body's immune system.'