Through epitope cross-reactivity, molecular mimicry between microbial and host antigens may help with autoimmunity as well as tumor protection. According to a recent study published in the journal Science, those cross-reactive epitopes may be caused by viruses that infect endogenous microbial species. & nbsp,
In this study, the authors made the unexpected finding that in an experimental cancer model, only a few Enterococcus hirae microbial strains( such as erections 13144 or IGR11 ) increased the anti-cancer effect.
The authors then demonstrated how this biological activity was connected to TSLARFANI, a dominant epitope derived from TMP protein that only appeared in 39.2 kb of prophage in those particular E. hirae strains. Mice that had been immunized with the heat-inactivated E. hirae 13144 strain, the TSLARFANI peptide, or an unrelated coli engineered to express TMP all had an enhanced anti-cancer effect. & nbsp,
The authors demonstrated that the epitope GSLARFRNI, which was derived from cancer cells used in these experiments, was recognized by the same CD8 T cells that labeled with TSLARFANI tetramers, confirming the cross-reactivity between these two endpoints.
This study concludes by arguing that the microbiota and bacteriophages they carry represent novel approaches to the fight against cancer. The overall anti-tumor effect in this study is modest, but we must remember that it only affects one type of MHC-inbred mice, and it is likely that many other epitopes will also play a role in outcrossed species like humans. Due to a lack of precise knowledge about human microbiota strains, as well as the poor dependability and performance of available bioinformatics approaches, it is still very difficult to conduct such analysis in humans in the real world scenario. However, it is much simpler to advance the field once the mechanistic principles underlying anti-cancer effects are discovered and accepted.
written by David Usharauli