Fcγ receptor IIA and IIIB polymorphisms are associated with susceptibility to cerebral malaria

Katsuse, Omi; Ohashi, Jun; Patarapotikul, Jintana; Hananantachai, Hathairad; Naka, Izumi; Looareesuwan, Sornchai; Tokunaga, Katsushi

doi:10.1016/s1383-5769(02)00040-5

Cited by 66 publications

(72 citation statements)

References 25 publications

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“…These genes show a substantial expressed SNP (eSNP) effect in the infected group or the control group but not in both, or show the effect in opposite directions in the two different groups. Other genes subject to interaction effects beneath genome-wide significance show different magnitudes of eSNP effects between the two groups and likely have important roles in modulating the course of infection, and several of them have previously been associated with malaria (i.e., FCGR3B, PSMB9, and GSTO1) (18)(19)(20). In addition, we discovered several associations implicating key immune processes, particularly antigen processing and presentation, plasmacytoid dendritic cell activation, and T-cell activation and expansion (i.e., RAD21, LRRC25, CLEC4C SLC3A2, and TAPBP) (21-25).…”

Section: Resultsmentioning

confidence: 99%

Evidence for additive and interaction effects of host genotype and infection in malaria

Idaghdour

Quinlan

Goulet

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

124

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The host mechanisms responsible for protection against malaria remain poorly understood, with only a few protective genetic effects mapped in humans. Here, we characterize a host-specific genome-wide signature in whole-blood transcriptomes of Plasmodium falciparum-infected West African children and report a demonstration of genotype-by-infection interactions in vivo. Several associations involve transcripts sensitive to infection and implicate complement system, antigen processing and presentation, and T-cell activation (i.e., SLC39A8, C3AR1, FCGR3B, RAD21, RETN, LRRC25, SLC3A2, and TAPBP), including one association that validated a genome-wide association candidate gene (SCO1), implicating binding variation within a noncoding regulatory element. Gene expression profiles in mice infected with Plasmodium chabaudi revealed and validated similar responses and highlighted specific pathways and genes that are likely important responders in both hosts. These results suggest that host variation and its interplay with infection affect children's ability to cope with infection and suggest a polygenic model mounted at the transcriptional level for susceptibility.host response | parasite load | eQTL | eSNP | genotype-by-environment interactions

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Section: Resultsmentioning

confidence: 99%

Evidence for additive and interaction effects of host genotype and infection in malaria

Idaghdour

Quinlan

Goulet

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

124

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“…CD36 directly mediates cytoadherence of Plasmodium falciparum parasitized erythrocytes and it binds long chain fatty acids and may function in the transport and/or as a regulator of fatty acid transport (Oquendo et al 1989;Baruch et al 1996;Erdman et al 2009). It was reported that CD36 has been subjected to positive selection for malaria or some unknown selection pressures (Aitman et al 2000;Omi et al 2002Omi et al , 2003Fry et al 2009). SEMA3C, induced by ADAMTS1, promotes the migration of cancer cells (Esselens et al 2010).…”

Section: Natural Selection In African Americansmentioning

confidence: 99%

Genome-wide detection of natural selection in African Americans pre- and post-admixture

Jin¹,

Xu²,

Wang³

et al. 2011

Genome Res.

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It is particularly meaningful to investigate natural selection in African Americans (AfA) due to the high mortality their African ancestry has experienced in history. In this study, we examined 491,526 autosomal single nucleotide polymorphisms (SNPs) genotyped in 5210 individuals and conducted a genome-wide search for selection signals in 1890 AfA. Several genomic regions showing an excess of African or European ancestry, which were considered the footprints of selection since population admixture, were detected based on a commonly used approach. However, we also developed a new strategy to detect natural selection both pre-and post-admixture by reconstructing an ancestral African population (AAF) from inferred African components of ancestry in AfA and comparing it with indigenous African populations (IAF). Interestingly, many selection-candidate genes identified by the new approach were associated with AfA-specific highrisk diseases such as prostate cancer and hypertension, suggesting an important role these disease-related genes might have played in adapting to a new environment. CD36 and HBB, whose mutations confer a degree of protection against malaria, were also located in the highly differentiated regions between AAF and IAF. Further analysis showed that the frequencies of alleles protecting against malaria in AAF were lower than those in IAF, which is consistent with the relaxed selection pressure of malaria in the New World. There is no overlap between the top candidate genes detected by the two approaches, indicating the different environmental pressures AfA experienced pre-and post-population admixture. We suggest that the new approach is reasonably powerful and can also be applied to other admixed populations such as Latinos and Uyghurs.

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“…Outside of Asia, the HH and RR genotypes each occur in ϳ25% of the population, and the RH genotype occurs in ϳ50% (23,24). There is marked skewing of this distribution in East Asia, where 50 -60% of individuals are H homozygotes and Ͻ10% carry the RR genotype (23,25,26).…”

Section: H Uman Immunodeficiency Virus (Hiv) Infection Is Char-mentioning

confidence: 99%

FcγRIIa Genotype Predicts Progression of HIV Infection

Forthal

Landucci

Bream

et al. 2007

The Journal of Immunology

119

129

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Polymorphisms in FcγR genes are associated with susceptibility to or severity of a number of autoimmune and infectious diseases. We found that HIV-infected men in the Multicenter AIDS Cohort Study with the FcγRIIa RR genotype progressed to a CD4+ cell count of <200/mm3 at a faster rate than individuals with the RH or HH genotypes (relative hazard = 1.6; p = 0.0001). However, progression to AIDS (using the broad definition of either a CD4+ cell count <200/mm3 or development of an AIDS-defining illness) was less impacted by FcγRIIa genotype, largely because HH homozygotes had an increased risk of Pneumocystis jiroveci pneumonia as an AIDS-defining illness. We also showed that chronically infected subjects develop a substantial anti-gp120-specific IgG2 response. Moreover, HIV-1 immune complexes are more efficiently internalized by monocytes from HH subjects compared with RR subjects, likely because of the presence of IgG2 in the complexes. Finally, the FcγRIIIa F/V gene polymorphism was not associated with progression of HIV infection, but, as demonstrated previously, did predict the risk of Kaposi’s sarcoma. These results demonstrate the importance of FcγRs in AIDS pathogenesis and point toward a critical role for interactions between FcγRs and immune complexes in disease progression.

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Fcγ receptor IIA and IIIB polymorphisms are associated with susceptibility to cerebral malaria

Cited by 66 publications

References 25 publications

Evidence for additive and interaction effects of host genotype and infection in malaria

Evidence for additive and interaction effects of host genotype and infection in malaria

Genome-wide detection of natural selection in African Americans pre- and post-admixture

FcγRIIa Genotype Predicts Progression of HIV Infection

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