What is it about?
The intracellular pathogen, Leishmania donovani in order to survive inside the macrophage successfully, needs to overcome thehost defence mechanisms, like the secretion of the pro-inflammatory cytokine, IL-1beta. IL-1beta is produced in its pro form which is activated by the inflammsome complex. Does the parasite inhibit the formation of the inflammasome complex? If so, then how?? This paper unravels the mechanism by which the mischievious parasite in order to evade the defence weaponry of the host cell exploits negative regulatory proteins of the host immune system.
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Why is it important?
Though various works have been done on the stealth mechanism of the parasite but this paper, to the best of our knowledge, is the first showing how the intracellular parasite evades the effects of the inflammasome complex in order to survive in the host cell. This work unravels the interplay between the parasite and the host and interestingly, how the parasite exploits the host negative regulatory proteins, A20 and UCP2 in order to thrive successfully within the host cell.
Perspectives
I hope that this article would help people understand the mechanisms exploited by certain intracellular pathogens in order to survive successfully and provide us an insight for futuristic therapeutic approaches against the menance of such pathogens.
Anand Gupta
Read the Original
This page is a summary of: Leishmania donovaniinhibits inflammasome-dependent macrophage activation by exploiting the negative regulatory proteins A20 and UCP2, The FASEB Journal, August 2017, Federation of American Societies For Experimental Biology (FASEB),
DOI: 10.1096/fj.201700407r.
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