Immune evasion of Plasmodium falciparum by RIFIN via inhibitory receptors
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Immune evasion of Plasmodium falciparum by RIFIN via inhibitory receptors. / Saito, Fumiji; Hirayasu, Kouyuki; Satoh, Takeshi; Wang, Christian W; Lusingu, John; Arimori, Takao; Shida, Kyoko; Palacpac, Nirianne Marie Q; Itagaki, Sawako; Iwanaga, Shiroh; Takashima, Eizo; Tsuboi, Takafumi; Kohyama, Masako; Suenaga, Tadahiro; Colonna, Marco; Takagi, Junichi; Lavstsen, Thomas; Horii, Toshihiro; Arase, Hisashi.
In: Nature, Vol. 552, No. 7683, 07.12.2017, p. 101-105.Research output: Contribution to journal › Letter › Research › peer-review
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TY - JOUR
T1 - Immune evasion of Plasmodium falciparum by RIFIN via inhibitory receptors
AU - Saito, Fumiji
AU - Hirayasu, Kouyuki
AU - Satoh, Takeshi
AU - Wang, Christian W
AU - Lusingu, John
AU - Arimori, Takao
AU - Shida, Kyoko
AU - Palacpac, Nirianne Marie Q
AU - Itagaki, Sawako
AU - Iwanaga, Shiroh
AU - Takashima, Eizo
AU - Tsuboi, Takafumi
AU - Kohyama, Masako
AU - Suenaga, Tadahiro
AU - Colonna, Marco
AU - Takagi, Junichi
AU - Lavstsen, Thomas
AU - Horii, Toshihiro
AU - Arase, Hisashi
N1 - Correction: Corrigendum: Immune evasion of Plasmodium falciparum by RIFIN via inhibitory receptors https://www.nature.com/articles/nature25498
PY - 2017/12/7
Y1 - 2017/12/7
N2 - 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.
AB - 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.
U2 - 10.1038/nature24994
DO - 10.1038/nature24994
M3 - Letter
C2 - 29186116
VL - 552
SP - 101
EP - 105
JO - Nature
JF - Nature
SN - 0028-0836
IS - 7683
ER -
ID: 186743233