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Chronic Malaria drives functional heterogenity in B cell subpopilations and expansion of unswitched atypical memory B cells

ABSTRACT: Chronic Malaria drives functional heterogenity in B cell subpopilations and expansion of unswitched atypical memory B cells

PROVIDER: PRJNA629804 | ENA |

REPOSITORIES: ENA

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Chronic Malaria drives functional heterogenity in B cell subpopilations and expansion of unswitched atypical memory B cells [Malaria scRNA-seq]

Project description:Human chronic infectious diseases have been shown to alter the composition and phenotype of the B cell compartment, which, in part, can attribute to failure to acquire protective immunity. However, the extent of such alterations is poorly understood. Here, using a combination of bulk and single cell RNA-sequencing (scRNA-seq) of B cells in individuals living in malaria-endemic Africa, we characterized changes in naïve B cell, classical memory B cell (MBC) and atypical MBC subsets. Of particular interest were unswitched atypical MBCs that expanded in children upon the onset of febrile malaria. This subpopulation expressed IgD but only low levels of IgM (IgD+IgMlo), high levels of the atypical MBC markers, Tbet and CD11c, as well as the intrinsically autoreactive VH4-34. IgD+IgMlo atypical MBCs were distinguished functionally by their acquisition of high antigen-affinity thresholds for activation, suggesting the IgD+IgMlo atypical MBC expansion during febrile malaria may reduce responses to low affinity self-antigens during acute malaria

2020-09-30 | GSE149728 | GEO

Chronic Malaria drives functional heterogenity in B cell subpopulations and expansion of unswitched atypical memory B cells [Malaria bulkRNA-seq]

2020-09-30 | GSE149727 | GEO

Chronic Malaria drives functional heterogenity in B cell subpopulations and expansion of unswitched atypical memory B cells [Malaria bulkRNA-seq]

Project description:Chronic Malaria drives functional heterogenity in B cell subpopulations and expansion of unswitched atypical memory B cells [Malaria bulkRNA-seq]

| PRJNA629811 | ENA

Chronic Malaria drives functional heterogenity in B cell subpopilations and expansion of unswitched atypical memory B cells [Malaria scRNA-seq]

Project description:Chronic Malaria drives functional heterogenity in B cell subpopilations and expansion of unswitched atypical memory B cells [Malaria scRNA-seq]

| PRJNA629812 | ENA

Malaria-associated atypical memory B cells exhibit markedly reduced B cell receptor signaling and effector function

Project description:Plasmodium falciparum malaria is a deadly infectious disease for which we have no licensed vaccine. Antibodies confer protection against malaria and individuals exposed to P. falciparum acquire protective antibodies, but only after years of repeated infections. We recently showed that malaria exposure is associated with a large expansion of a population of atypical memory B cells (MBCs) that phenotypically resemble B cell populations expanded in chronic viral infections, including HIV. At present the relationship of atypical MBCs to classical MBCs and their function are not known. We provide evidence that the expressed VH gene repertoires and somatic hypermutation rates of atypical and classical MBCs are indistinguishable, indicating the two populations are closely related developmentally. Atypical MBCs can be distinguished by their expression of multiple inhibitory receptors, including Fc receptor-like-5. B cell receptor (BCR) signaling is stunted in atypical MBCs, resulting in impaired Ca2+ mobilization, proliferation and cytokine production. Atypical MBCs do not spontaneously secrete antibodies and cannot be stimulated to differentiate into antibody-secreting cells in vitro. These results suggest that in individuals chronically exposed to malaria, atypical MBCs differentiate from classical MBCs and assume a phenotype refractory to BCR-mediated activation, potentially contributing to the inefficient acquisition of immunity to malaria. Comparison of human atypical B cell versus classical B cell versus naïve B cell.

2015-05-07 | E-GEOD-65928 | biostudies-arrayexpress

Shared transcriptional profiles at the single cell level of atypical memory B cells suggest common drivers of expansion and function in malaria, HIV and autoimmune diseases [HIV scRNA-seq]

Project description:Human chronic infectious diseases, including malaria and HIV and autoimmune diseases, notably SLE, are accompanied by a striking expansion of a subpopulation of B cells termed atypical memory B cells (MBCs). We compared the single cell transcriptional profiles of B cells in malaria and HIV, characterizing and uncovering heterogeneity within each B cell subset. Remarkably, atypical MBC clusters in these two diseases showed significant similarities to each other as well as to atypical MBCs in autoimmune diseases, suggesting a common driver of their expansion and shared functions. Focusing on atypical MBCs in malaria we identified an IgD+IgMlo subpopulation that expanded in children upon the onset of febrile malaria, showed a distinct V gene usage characteristic of antigen-driven B cell populations and unexpectedly, had acquired high antigen-affinity thresholds for activation. We speculate that in malaria IgD+IgMlo atypical MBCs expand to limit responses to low-affinity self-antigens, a function that may be shared by atypical MBCs in other chronic infections and autoimmune diseases.

2020-09-30 | GSE157966 | GEO

Shared transcriptional profiles at the single cell level of atypical memory B cells suggest common drivers of expansion and function in malaria, HIV and autoimmune diseases [Malaria VDJ+GEX scRNA-seq]

2020-09-30 | GSE157967 | GEO

Malaria-associated atypical memory B cells exhibit markedly reduced B cell receptor signaling and effector function

2015-05-07 | GSE65928 | GEO

Expansion of an FCRL5+ B cell subset resembling atypical memory B cells in an animal model of malaria

Project description:Background: In human malaria, parasites of the genus Plasmodium elicit expansion of atypical memory B cells (atMBCs), which lack the classical markers CD21 and CD27. We have identified a putative population of analogous B cells in a murine model of infection with P. chabaudi, delineated by the marker FCRL5. We performed RNA-Seq on FCRL5+ and FCRL5- B cells sorted from infected mice, so as to characterize the transcriptional profile of these cells and permit comparison to atMBCs in humans. Results: FCRL5+ B cells were found to have distinct transcriptional profiles from FCRL5- B cells, with approximately 400 genes exhibiting significant differences between the two groups. Additionally, about 25% of these differentially expressed genes were also differentially expressed in human atMBCs versus classical MBCs, as previously described by Sullivan et al (PLoS Pathogens 2015). Conclusions: FCRL5+ class-switched B cells are a transcriptionally distinct subset arising in P. chabaudi infection, with transcriptional similarities to human atMBCs that develop in chronic malaria settings.

2019-04-16 | GSE85205 | GEO

Chronic Malaria drives functional heterogenity in B cell subpopilations and expansion of unswitched atypical memory B cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-30 | GSE149729 | GEO