There are 60 million people in the US – and billions in the rest of the world – infected with the parasite that causes toxoplasmosis. The infection rarely causes symptoms, but in pregnant women and those with weakened immune systems, it can flare up and cause significant health problems. As yet, there is no vaccine, but scientists are closing in on one.
Now, a new study – by researchers at Osaka University in Japan and published in the journal Cell Reports – identifies a molecule in human cells that could be important for triggering the appropriate immune reaction from an effective vaccine for the single-celled parasite, which is called Toxoplasma gondii.
Infection with Toxoplasma can cause fatal encephalosis or pneumonia in patients receiving treatment for AIDS or cancer, whose immune systems are weak. It can also trigger miscarriage in pregnant women or cause their child to be born with a congenital disease.
The parasite is transmitted through raw meat containing T. gondii cysts or water containing oocysts from cat feces.
The team behind the new study, headed by Masahiro Yamamoto, a professor at a research institute for microbial diseases and immunology at Osaka, used mice to explore how their cells react to an experimental vaccine based on inactivated Toxoplasma.
They found that a large host molecule called p62 plays an important role in triggering the immune system in Toxoplasma infection.
The team hopes the finding will lead to vaccines that target p62 for preventing parasite infection. The authors note that cases of toxoplasmosis are on the rise in Japan.
The discovery concerns what happens inside cells infected with the parasite. The parasite infects cells by creating “vacuoles,” or small pockets in the fluid surrounding the cell nucleus.
In the vacuoles, the parasite releases antigens, which can be recognized and targeted by killer T cells of the immune system. The killer T cells are themselves stimulated by the cytokine interferon-γ (IFN-γ) – a type of protein that coordinates cellular programs by switching genes on and off.
The team compared Toxoplasma-infected cells where the immune system was stimulated by IFN-γ with those where it was not. They found that levels of killer T cells that were specific to Toxoplasma were higher in infected cells where the immune system was triggered by IFN-γ.
They then showed that p62 is important for the stronger IFN-γ-elicited immune response – because in mice lacking the molecule, the antigen-specific killer T cell count was significantly reduced.
Progress is also being made toward more effective treatments for toxoplasmosis. For example, in January 2014, Medical News Today reported how a new protein discovery could help treat toxoplasmosis. A study led by Indiana University School of Medicine and published in PLOS Pathogens identified a protein called GCN5b – that is active in both undeveloped and severe forms of toxoplasmosis – as a potential drug target.