Parasite disguises itself with human proteins to evade immune system

Amazing stuff! Very clever!

"Parasites are known to infect human cells through a variety of ingenious mechanisms. Many of them have even evolved sophisticated strategies to evade a host’s immune system by avoiding it entirely.

One type of parasite, Entamoeba histolytica, has developed a very intriguing way to do this. It rips pieces off human cells and steals the proteins to wear them as a disguise. ...

Instead of ingesting cells in such a way that will kill them, this parasite bites chunks off the cells and leaves them wounded. But it doesn’t merely eat these pieces for food; it steals their proteins, namely CD46 and CD55, from the outer membrane of the cell and cloaks them around its own surface. These two proteins are used to shield human cells from being attacked by the immune system.

With the integration of proteins around itself, the immune system’s defenses assume E.  histolytica is a part of the host, allowing amoebae to remain invisible. This process of taking another cell's proteins is called trogocytosis. ..."

From the abstract:

"Entamoeba histolytica is a major cause of diarrheal disease. E. histolytica trophozoites (“amoebae”) can invade the intestine and disseminate via the bloodstream, resisting complement lysis through unknown mechanisms. Amoebae kill human cells by performing trogocytosis. After performing trogocytosis, amoebae display human proteins on their own surface and are resistant to lysis by human serum.

In this study we sought to further evaluate the mechanism by which amoebae resist complement. To test if complement is responsible for lysis of amoebae, C3-depleted serum was compared to replete serum, and C3 was required for lysis. Amoebae were allowed to perform trogocytosis of human cells and exposed to mouse serum. Although they had performed trogocytosis on a different species than the source of the serum, they were protected from lysis. To test if the protection from lysis by mouse serum was due to the functional interchangeability of human and mouse complement pathway proteins, human CD46 or CD55 (negative regulators of complement activation) were exogenously expressed. Amoebae that expressed human CD46 or CD55 were protected from lysis by mouse serum, indicating that display of human proteins was sufficient to inhibit mouse complement activation.

Finally, amoebae were allowed to perform trogocytosis of a cell type in which the complement pathway is not conserved, and they did not become resistant to lysis. Overall, these findings are consistent with the model that trogocytosis enables amoebic acquisition and display of host proteins, including negative regulators of the complement pathway, that provide protection from complement lysis. Since other microbes can perform trogocytosis, this novel mechanism for complement resistance might apply to other infections."

Parasite disguises itself with human proteins to evade immune system

Wily Parasite Kills Human Cells and Wears Their Remains as Disguise

Cross-species protection suggests Entamoeba histolytica trogocytosis enables complement resistance through the transfer of negative regulators of complement activation (open access)

Fig. 2 Trogocytosis of human cells protects amoebae from lysis by mouse serum.

Entamoeba histolytica is a single-cell parasite that causes intestinal disease, but sometimes invades the body, attacking cells and creating liquefying abscesses. ... Image shows E. histolytica (green) attacking human T-cells (white blood cells). 

Katherine Ralston parasitologist