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Fc receptor-like 4 (FCLR4) and Fc receptor-like receptor 5 (FCRL5) define and control human atypical memory B cells [array]

ABSTRACT: Fc receptor-like 4 (FCLR4) and Fc receptor-like receptor 5 (FCRL5) define and control human atypical memory B cells [array]

PROVIDER: PRJNA602722 | ENA |

REPOSITORIES: ENA

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Fc receptor-like 4 (FCLR4) and Fc receptor-like receptor 5 (FCRL5) define and control human atypical memory B cells

Project description:Fc receptor-like 4 (FCLR4) and Fc receptor-like receptor 5 (FCRL5) define and control human atypical memory B cells

| PRJNA607470 | ENA

Fc receptor-like 4 (FCLR4) and Fc receptor-like receptor 5 (FCRL5) define and control human atypical memory B cells [RNA-Seq]

Project description:Fc receptor-like 4 (FCLR4) and Fc receptor-like receptor 5 (FCRL5) define and control human atypical memory B cells [RNA-Seq]

| PRJNA607491 | ENA

Fc receptor-like 4 (FCLR4) and Fc receptor-like receptor 5 (FCRL5) define and control human atypical memory B cells [RNA-Seq]

Project description:We performed NGS on Ig heavy chain V sequences amplified from RNA obtained from human tonsillar B cell subsets. From these NGS data, we reconstructed ongoing B cell responses as lineage trees, providing crucial in vivo developmental context. Each memory subset typically maintained its lineage, denoting mechanisms enforcing their phenotypes. FCRL4-FCRL5+ cells were the most represented memory subset in lineage trees, indicating robust participation in ongoing responses. Affinity maturation of both FCRL4-FCRL5+ and FCRL4+FCRL5+ atypical memory cells was stalled in chronic streptococcus infection, conceivably due to negative feedback from IgG immune complexes. We propose that FCRL4 and FCRL5 function as sensors of immune complexes, thus controlling atypical memory B cell responses.

2020-08-04 | GSE145519 | GEO

Fc receptor-like 4 (FCLR4) and Fc receptor-like receptor 5 (FCRL5) define and control human atypical memory B cells [array]

Project description:We performed gene array analysis of three memnory cell subsets sorted from three tonsil donors with the following patterns of surface expression: FCRL4-, FCRL5+ (designated F5), FCRL4 -, FCRL 5- (designated DN) , and FCRL4+, FCRL5+ (designated DP). The three memory subsets were clearly segregated by principal component analysis and cluster analysis as distinct, and hundreds of genes were found differentially expressed. between any two subsets

2020-08-04 | GSE144089 | GEO

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

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

Fc receptor-like 4 (FCLR4) and Fc receptor-like receptor 5 (FCRL5) define and control human atypical memory B cells

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

2020-08-04 | GSE145520 | GEO

The Paired Orphan Immune Receptors LILRA6 and LILRB3 Modulate Fc Receptor Mediated Functions of Neutrophils

Project description:to characterise expression of LILRA6/LILRB3 receptors during neutrophil differentiation and activation, and to characterise their roles in modulating Fc receptor mediated effector functions.

2020-11-04 | PXD015561 | Pride

Plasmodium-specific atypical memory B cells are short-lived activated B cells

Project description:Chronic infections such as HIV, tuberculosis and malaria in humans are associated with the appearance of atypical memory B cells in peripheral blood. It has been suggested that these B cells do not function normally as memory cells, and thus may be responsible for poor acquisition of immunity and maintenance of chronic infections. Studies on these cells in human infections are limited by the lack of accessibility to lymphoid organs, and relevant mouse models would be valuable to investigate their development, functional capacities, and role. To investigate Plasmodium-specific memory B-cell responses during malaria, we generated an immunoglobin heavy chain knock-in mouse with a B-cell receptor that recognizes the merozoite surface protein (MSP)-1 of the rodent malaria parasite, Plasmodium chabaudi. Using this mouse and a P. chabaudi infection initiated by infected mosquito bites we show that antigen-specific B cells with many characteristics of human atypical memory B cells are generated. These cells are immunoglobulin class-switched and express, among others, the cell surface molecules CD11c, CD11b, FCRL5, and some inhibitory receptors including PD1 and LAIR-1, as well as the transcription factor T-bet. Antigen-specific atypical memory B cells are detected side-by-side with classical memory B cells during chronic blood-stage infection. Whereas classical memory B cells persist after complete infection clearance, atypical memory B cells are short-lived and disappear from the spleen at the resolution of chronic infection. Short-lived Plasmodium-specific atypical B cells also appear transiently after immunization with a TLR7/8 ligand and MSP-1. Our data suggest that these atypical memory B cells are not a subset of memory B cells, but rather antigen-experienced activated cells, and part of a normal ongoing response. Their persistence over weeks in malaria and other infections may be a consequence of continued and chronic antigenic stimulation.

2018-11-01 | GSE115155 | GEO

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