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Limited access to antigen drives the generation of early B cell memory while restraining the plasmablast response

ABSTRACT: Limited access to antigen drives the generation of early B cell memory while restraining the plasmablast response

PROVIDER: PRJNA732379 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14631700_1.fastq.gz	Fastqsanger.gz
	SRR14631700_2.fastq.gz	Fastqsanger.gz
	SRR14631701_1.fastq.gz	Fastqsanger.gz
	SRR14631701_2.fastq.gz	Fastqsanger.gz
	SRR14631702_1.fastq.gz	Fastqsanger.gz

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Limited access to antigen drives the generation of early B cell memory while restraining the plasmablast response

Project description:The cell fate decisions between plasmablasts (PBs), germinal center B cells (GCBCs) and non-GC-derived memory B cells (MBCs) during early B cell activation determine the outcome of the immune responses to pathogens and vaccines. In this study, we dissected these poorly characterized lineage choices by single-cell RNA-sequencing. Early after immunization, a homogenous population of activated precursors (APs) gave rise to a transient wave of PBs, followed a day later by the emergence of the first GCBCs, with the transcriptomes of both rapidly diverging from that of APs. The majority of APs started to withdraw from the cell cycle very early on and gave rise to GC-independent MBCs, a developmental transition that involved limited transcriptional changes. These events were controlled by antigen availability, and provision of antigen excess interfered with cell cycle exit and induced a new wave of PBs. Fate mapping experiments revealed a prominent contribution of GC-independent memory to the overall MBC pool. Quiescent cells with an MBC phenotype also dominated the early response to immunization in primates, indicating evolutionary conservation. Thus, excess APs, kept in reserve as early MBCs, can be rapidly re-recruited if failure to contain a threat is manifested by increased antigen availability, thus providing a feedback mechanism for rapid readjustment of the immune response.

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Limited access to antigen drives generation of early B cell memory while restraining the plasmablast response.

Project description:Cell fate decisions during early B cell activation determine the outcome of responses to pathogens and vaccines. We examined the early B cell response to T-dependent antigen in mice by single-cell RNA sequencing. Early after immunization, a homogeneous population of activated precursors (APs) gave rise to a transient wave of plasmablasts (PBs), followed a day later by the emergence of germinal center B cells (GCBCs). Most APs rapidly exited the cell cycle, giving rise to non-GC-derived early memory B cells (eMBCs) that retained an AP-like transcriptional profile. Rapid decline of antigen availability controlled these events; provision of excess antigen precluded cell cycle exit and induced a new wave of PBs. Fate mapping revealed a prominent contribution of eMBCs to the MBC pool. Quiescent cells with an MBC phenotype dominated the early response to immunization in primates. A reservoir of APs/eMBCs may enable rapid readjustment of the immune response when failure to contain a threat is manifested by increased antigen availability.

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