Literature DB >> 32066522

Plasmodium-infected erythrocytes induce secretion of IGFBP7 to form type II rosettes and escape phagocytosis.

Wenn-Chyau Lee1, Bruce Russell2, Radoslaw Mikolaj Sobota3,4, Khairunnisa Ghaffar1, Shanshan W Howland1, Zi Xin Wong1, Alexander G Maier5, Dominique Dorin-Semblat6,7, Subhra Biswas1, Benoit Gamain6,7, Yee-Ling Lau8, Benoit Malleret1,9, Cindy Chu10,11, François Nosten10,11, Laurent Renia1.   

Abstract

In malaria, rosetting is described as a phenomenon where an infected erythrocyte (IRBC) is attached to uninfected erythrocytes (URBC). In some studies, rosetting has been associated with malaria pathogenesis. Here, we have identified a new type of rosetting. Using a step-by-step approach, we identified IGFBP7, a protein secreted by monocytes in response to parasite stimulation, as a rosette-stimulator for Plasmodium falciparum- and P. vivax-IRBC. IGFBP7-mediated rosette-stimulation was rapid yet reversible. Unlike type I rosetting that involves direct interaction of rosetting ligands on IRBC and receptors on URBC, the IGFBP7-mediated, type II rosetting requires two additional serum factors, namely von Willebrand factor and thrombospondin-1. These two factors interact with IGFBP7 to mediate rosette formation by the IRBC. Importantly, the IGFBP7-induced type II rosetting hampers phagocytosis of IRBC by host phagocytes.
© 2020, Lee et al.

Entities:  

Keywords:  IGFBP7; P. falciparum; P. vivax; host-parasite interaction; immunology; infectious disease; inflammation; microbiology; phagocytosis; rosette

Mesh:

Substances:

Year:  2020        PMID: 32066522      PMCID: PMC7048393          DOI: 10.7554/eLife.51546

Source DB:  PubMed          Journal:  Elife        ISSN: 2050-084X            Impact factor:   8.140


  76 in total

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