Shed EBA-175 mediates red blood cell clustering that enhances malaria parasite growth and enables immune evasion

Research output: Contribution to journalJournal articleResearchpeer-review

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Shed EBA-175 mediates red blood cell clustering that enhances malaria parasite growth and enables immune evasion. / Paing, May M; Salinas, Nichole D; Adams, Yvonne; Oksman, Anna; Jensen, Anja TR; Goldberg, Daniel E; Tolia, Niraj H.

In: eLife, Vol. 7, e43224, 2018.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Paing, MM, Salinas, ND, Adams, Y, Oksman, A, Jensen, ATR, Goldberg, DE & Tolia, NH 2018, 'Shed EBA-175 mediates red blood cell clustering that enhances malaria parasite growth and enables immune evasion', eLife, vol. 7, e43224. https://doi.org/10.7554/eLife.43224

APA

Paing, M. M., Salinas, N. D., Adams, Y., Oksman, A., Jensen, A. TR., Goldberg, D. E., & Tolia, N. H. (2018). Shed EBA-175 mediates red blood cell clustering that enhances malaria parasite growth and enables immune evasion. eLife, 7, [e43224]. https://doi.org/10.7554/eLife.43224

Vancouver

Paing MM, Salinas ND, Adams Y, Oksman A, Jensen ATR, Goldberg DE et al. Shed EBA-175 mediates red blood cell clustering that enhances malaria parasite growth and enables immune evasion. eLife. 2018;7. e43224. https://doi.org/10.7554/eLife.43224

Author

Paing, May M ; Salinas, Nichole D ; Adams, Yvonne ; Oksman, Anna ; Jensen, Anja TR ; Goldberg, Daniel E ; Tolia, Niraj H. / Shed EBA-175 mediates red blood cell clustering that enhances malaria parasite growth and enables immune evasion. In: eLife. 2018 ; Vol. 7.

Bibtex

@article{72385a884b534686b7cc6731a0cd559e,
title = "Shed EBA-175 mediates red blood cell clustering that enhances malaria parasite growth and enables immune evasion",
abstract = "Erythrocyte Binding Antigen of 175 kDa (EBA-175) has a well-defined role in binding to glycophorin A (GpA) during Plasmodium falciparum invasion of erythrocytes. However, EBA-175 is shed post invasion and a role for this shed protein has not been defined. We show that EBA-175 shed from parasites promotes clustering of RBCs, and EBA-175-dependent clusters occur in parasite culture. Region II of EBA-175 is sufficient for clustering RBCs in a GpA-dependent manner. These clusters are capable of forming under physiological flow conditions and across a range of concentrations. EBA-175-dependent RBC clustering provides daughter merozoites ready access to uninfected RBCs enhancing parasite growth. Clustering provides a general method to protect the invasion machinery from immune recognition and disruption as exemplified by protection from neutralizing antibodies that target AMA-1 and RH5. These findings provide a mechanistic framework for the role of shed proteins in RBC clustering, immune evasion, and malaria.",
author = "Paing, {May M} and Salinas, {Nichole D} and Yvonne Adams and Anna Oksman and Jensen, {Anja TR} and Goldberg, {Daniel E} and Tolia, {Niraj H}",
year = "2018",
doi = "10.7554/eLife.43224",
language = "English",
volume = "7",
journal = "eLife",
issn = "2050-084X",
publisher = "eLife Sciences Publications Ltd.",

}

RIS

TY - JOUR

T1 - Shed EBA-175 mediates red blood cell clustering that enhances malaria parasite growth and enables immune evasion

AU - Paing, May M

AU - Salinas, Nichole D

AU - Adams, Yvonne

AU - Oksman, Anna

AU - Jensen, Anja TR

AU - Goldberg, Daniel E

AU - Tolia, Niraj H

PY - 2018

Y1 - 2018

N2 - Erythrocyte Binding Antigen of 175 kDa (EBA-175) has a well-defined role in binding to glycophorin A (GpA) during Plasmodium falciparum invasion of erythrocytes. However, EBA-175 is shed post invasion and a role for this shed protein has not been defined. We show that EBA-175 shed from parasites promotes clustering of RBCs, and EBA-175-dependent clusters occur in parasite culture. Region II of EBA-175 is sufficient for clustering RBCs in a GpA-dependent manner. These clusters are capable of forming under physiological flow conditions and across a range of concentrations. EBA-175-dependent RBC clustering provides daughter merozoites ready access to uninfected RBCs enhancing parasite growth. Clustering provides a general method to protect the invasion machinery from immune recognition and disruption as exemplified by protection from neutralizing antibodies that target AMA-1 and RH5. These findings provide a mechanistic framework for the role of shed proteins in RBC clustering, immune evasion, and malaria.

AB - Erythrocyte Binding Antigen of 175 kDa (EBA-175) has a well-defined role in binding to glycophorin A (GpA) during Plasmodium falciparum invasion of erythrocytes. However, EBA-175 is shed post invasion and a role for this shed protein has not been defined. We show that EBA-175 shed from parasites promotes clustering of RBCs, and EBA-175-dependent clusters occur in parasite culture. Region II of EBA-175 is sufficient for clustering RBCs in a GpA-dependent manner. These clusters are capable of forming under physiological flow conditions and across a range of concentrations. EBA-175-dependent RBC clustering provides daughter merozoites ready access to uninfected RBCs enhancing parasite growth. Clustering provides a general method to protect the invasion machinery from immune recognition and disruption as exemplified by protection from neutralizing antibodies that target AMA-1 and RH5. These findings provide a mechanistic framework for the role of shed proteins in RBC clustering, immune evasion, and malaria.

U2 - 10.7554/eLife.43224

DO - 10.7554/eLife.43224

M3 - Journal article

C2 - 30556808

VL - 7

JO - eLife

JF - eLife

SN - 2050-084X

M1 - e43224

ER -

ID: 210836012