proteins are responsible for the production of interferon gamma, an important protein that helps launch a full-blown immune system attack against foreign pathogens.
A group of mice with both STAT1 and T-bet genes intact served as a control.
About two weeks after infection, the researchers began measuring the number of L. donovani parasites in the animals’ livers.
The pathogen went wild in the mice that lacked T-bet – the researchers found thousands upon thousands of the parasites in the livers of these animals.
Yet there were next to no parasites in the mice without STAT1.
‘Two weeks after infection, the mice without STAT1 had 25-fold fewer parasites in their liver tissue than the normal mice, and about 100-fold fewer parasites than the mice without T-bet,’ Satoskar said. ‘Visceral leishmaniasis never developed in the animals without STAT1 – the parasites weren’t able to establish an infection in the animals’ livers and spleens.’
The researchers also measured parasite levels in the livers two months after infection. Again, levels were quite high in the mice without T-bet, while normal mice and mice without STAT1 showed no sign of the disease.
While the normal mice weren’t sick – they showed no physical signs of having leishmaniasis, such as inflammation of the liver and spleen – Satoskar said the parasite was still in their systems.
‘Once infected, the parasite never goes away completely,’ Satoskar said. ‘It’s always hiding somewhere.’
Ironically, L. donovani thrives in the liver and spleen by infecting the very cells that the immune system uses to rid the parasite from the body. These cells are called macrophages – a kind of garbage collector for the immune system, as they clean out everything from red blood cells that have died to infectious pathogens. But enough L. donovani parasites can overtake a macrophage’s ability to clean up.
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