Nature communications · 2021
Malaria parasites both repress host CXCL10 and use it as a cue for growth acceleration.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Ошибки и ограничения
История · было → стало
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Ofir-Birin Yifat, Ben Ami Pilo Hila, Cruz Camacho Abel, Rudik Ariel, Rivkin Anna, Revach Or-Yam, Nir Netta, Block Tamin Tal, Abou Karam Paula, Kiper Edo, Peleg Yoav, Nevo Reinat, Solomon Aryeh, Havkin-Solomon Tal, Rojas Alicia, Rotkopf Ron, Porat Ziv, Avni Dror, Schwartz Eli, Zillinger Thomas, Hartmann Gunther, Di Pizio Antonella, Quashie Neils Ben, Dikstein Rivka, Gerlic Motti, Torrecilhas Ana Claudia, Levy Carmit, Nolte-'t Hoen Esther N M, Bowie Andrew G, Regev-Rudzki Neta
Аннотация
Pathogens are thought to use host molecular cues to control when to initiate life-cycle transitions, but these signals are mostly unknown, particularly for the parasitic disease malaria caused by Plasmodium falciparum. The chemokine CXCL10 is present at high levels in fatal cases of cerebral malaria patients, but is reduced in patients who survive and do not have complications. Here we show a Pf 'decision-sensing-system' controlled by CXCL10 concentration. High CXCL10 expression prompts P. falciparum to initiate a survival strategy via growth acceleration. Remarkably, P. falciparum inhibits CXCL10 synthesis in monocytes by disrupting the association of host ribosomes with CXCL10 transcripts. The underlying inhibition cascade involves RNA cargo delivery into monocytes that triggers RIG-I, which leads to HUR1 binding to an AU-rich domain of the CXCL10 3'UTR. These data indicate that when the parasite can no longer keep CXCL10 at low levels, it can exploit the chemokine as a cue to shift tactics and escape.