Lack of Association of CD55 Receptor Genetic Variants and Severe Malaria in Ghanaian Children

Schuldt, Kathrin; Ehmen, Christa; Sievertsen, Juergen; Evans, Jennifer; May, Jürgen; Ansong, Daniel; Muntau, Birgit; Ruge, Gerd; Timmann, Christian; Agbenyega, Tsiri; Horstmann, Rolf D.; Thye, Thorsten

doi:10.1534/g3.116.036475

Cited by 5 publications

(4 citation statements)

References 24 publications

(37 reference statements)

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“…1C and fig. S2A) ( 21 ). We also validated by flow cytometry an increase in the intracellular expression of Ezrin in ABCs as compared to naïve B cells and classic MBCs ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Shared transcriptional profiles of atypical B cells suggest common drivers of expansion and function in malaria, HIV, and autoimmunity

et al. 2021

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Chronic infectious diseases have a substantial impact on the human B cell compartment including a notable expansion of B cells here termed atypical B cells (ABCs). Using unbiased single-cell RNA sequencing (scRNA-seq), we uncovered and characterized heterogeneities in naïve B cell, classical memory B cells, and ABC subsets. We showed remarkably similar transcriptional profiles for ABC clusters in malaria, HIV, and autoimmune diseases and demonstrated that interferon-γ drove the expansion of ABCs in malaria. These observations suggest that ABCs represent a separate B cell lineage with a common inducer that further diversifies and acquires disease-specific characteristics and functions. In malaria, we identified ABC subsets based on isotype expression that differed in expansion in African children and in B cell receptor repertoire characteristics. Of particular interest, IgD+IgMlo and IgD−IgG+ ABCs acquired a high antigen affinity threshold for activation, suggesting that ABCs may limit autoimmune responses to low-affinity self-antigens in chronic malaria.

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“…1C and fig. S2A) ( 21 ). We also validated by flow cytometry an increase in the intracellular expression of Ezrin in ABCs as compared to naïve B cells and classic MBCs ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Shared transcriptional profiles of atypical B cells suggest common drivers of expansion and function in malaria, HIV, and autoimmunity

et al. 2021

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“…The basigin polymorphism that defines the Ok blood group has been associated with the efficiency of binding of the PfRh5 ligand (Crosnier et al, 2011). However, the major polymorphism of CD55 found in African populations is not associated with disease severity (Schuldt et al, 2017).…”

Section: Powering Invasionmentioning

confidence: 99%

The Molecular Basis of Erythrocyte Invasion by Malaria Parasites

Cowman

Tonkin

Tham

et al. 2017

Cell Host & Microbe

262

286

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Plasmodium species cause malaria by proliferating in human erythrocytes. Invasion of immunologically privileged erythrocytes provides a relatively protective niche as well as access to a rich source of nutrients. Plasmodium spp. target erythrocytes of different ages, but share a common mechanism of invasion. Specific engagement of erythrocyte receptors defines target cell tropism, activating downstream events and resulting in the physical penetration of the erythrocyte, powered by the parasite's actinomyosin-based motor. Here we review the latest in our understanding of the molecular composition of this highly complex and fascinating biological process.

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“…This is an aggregated African population, since finer scale surveys of different global populations are not available. Attempts to find a link between severe malaria outcomes and CD55 [44] or basigin [45] associated SNPs have so far failed [44,45].…”

Section: Discussionmentioning

confidence: 99%

Adaptive immunity selects against malaria infection blocking mutations

Penman¹,

Gandon²

2020

PLoS Comput Biol

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The mutation responsible for Duffy negativity, which impedes Plasmodium vivax infection, has reached high frequencies in certain human populations. Conversely, mutations capable of blocking the more lethal P. falciparum have not succeeded in malarious zones. Here we present an evolutionary-epidemiological model of malaria which demonstrates that if adaptive immunity against the most virulent effects of malaria is gained rapidly by the host, mutations which prevent infection per se are unlikely to succeed. Our results (i) explain the rarity of strain-transcending P. falciparum infection blocking adaptations in humans; (ii) make the surprising prediction that mutations which block P. falciparum infection are most likely to be found in populations experiencing low or infrequent malaria transmission, and (iii) predict that immunity against some of the virulent effects of P. vivax malaria may be built up over the course of many infections.

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Lack of Association of CD55 Receptor Genetic Variants and Severe Malaria in Ghanaian Children

Cited by 5 publications

References 24 publications

Shared transcriptional profiles of atypical B cells suggest common drivers of expansion and function in malaria, HIV, and autoimmunity

Shared transcriptional profiles of atypical B cells suggest common drivers of expansion and function in malaria, HIV, and autoimmunity

The Molecular Basis of Erythrocyte Invasion by Malaria Parasites

Adaptive immunity selects against malaria infection blocking mutations

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