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Immune evasion of Plasmodium falciparum by RIFIN via inhibitory receptors

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  • nihms917788

    Accepteret manuskript, 5,25 MB, PDF-dokument

  • Fumiji Saito
  • Kouyuki Hirayasu
  • Takeshi Satoh
  • Wang, Christian William
  • John Lusingu
  • Takao Arimori
  • Kyoko Shida
  • Nirianne Marie Q Palacpac
  • Sawako Itagaki
  • Shiroh Iwanaga
  • Eizo Takashima
  • Takafumi Tsuboi
  • Masako Kohyama
  • Tadahiro Suenaga
  • Marco Colonna
  • Junichi Takagi
  • Lavstsen, Thomas
  • Toshihiro Horii
  • Hisashi Arase

Malaria is among the most serious infectious diseases affecting humans, accounting for approximately half a million deaths each year. Plasmodium falciparum causes most life-threatening cases of malaria. Acquired immunity to malaria is inefficient, even after repeated exposure to P. falciparum, but the immune regulatory mechanisms used by P. falciparum remain largely unknown. Here we show that P. falciparum uses immune inhibitory receptors to achieve immune evasion. RIFIN proteins are products of a polymorphic multigene family comprising approximately 150-200 genes per parasite genome that are expressed on the surface of infected erythrocytes. We found that a subset of RIFINs binds to either leucocyte immunoglobulin-like receptor B1 (LILRB1) or leucocyte-associated immunoglobulin-like receptor 1 (LAIR1). LILRB1-binding RIFINs inhibit activation of LILRB1-expressing B cells and natural killer (NK) cells. Furthermore, P. falciparum-infected erythrocytes isolated from patients with severe malaria were more likely to interact with LILRB1 than erythrocytes from patients with non-severe malaria, although an extended study with larger sample sizes is required to confirm this finding. Our results suggest that P. falciparum has acquired multiple RIFINs to evade the host immune system by targeting immune inhibitory receptors.

OriginalsprogEngelsk
TidsskriftNature
Vol/bind552
Udgave nummer7683
Sider (fra-til)101-105
Antal sider5
ISSN0028-0836
DOI
StatusUdgivet - 7 dec. 2017

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