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High-affinity, neutralizing antibodies to SARS-CoV-2 can be made in the absence of T follicular helper cells

ABSTRACT: High-affinity, neutralizing antibodies to SARS-CoV-2 can be made in the absence of T follicular helper cells

PROVIDER: PRJNA780318 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16943421_1.fastq.gz	Fastqsanger.gz
	SRR16943421_2.fastq.gz	Fastqsanger.gz
	SRR16943422_1.fastq.gz	Fastqsanger.gz
	SRR16943422_2.fastq.gz	Fastqsanger.gz
	SRR16943423_1.fastq.gz	Fastqsanger.gz

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High-affinity, neutralizing antibodies to SARS-CoV-2 can be made without T follicular helper cells.

Project description:T follicular helper (TFH) cells are the conventional drivers of protective, germinal center (GC)–based antiviral antibody responses. However, loss of TFH cells and GCs has been observed in patients with severe COVID-19. As T cell–B cell interactions and immunoglobulin class switching still occur in these patients, noncanonical pathways of antibody production may be operative during SARS-CoV-2 infection. We found that both TFH-dependent and -independent antibodies were induced against SARS-CoV-2 infection, SARS-CoV-2 vaccination, and influenza A virus infection. Although TFH-independent antibodies to SARS-CoV-2 had evidence of reduced somatic hypermutation, they were still high affinity, durable, and reactive against diverse spike-derived epitopes and were capable of neutralizing both homologous SARS-CoV-2 and the B.1.351 (beta) variant of concern. We found by epitope mapping and B cell receptor sequencing that TFH cells focused the B cell response, and therefore, in the absence of TFH cells, a more diverse clonal repertoire was maintained. These data support an alternative pathway for the induction of B cell responses during viral infection that enables effective, neutralizing antibody production to complement traditional GC-derived antibodies that might compensate for GCs damaged by viral inflammation.

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High-affinity, neutralizing antibodies to SARS-CoV-2 can be made in the absence of T follicular helper cells

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Project description:SARS-CoV-2 has spread globally and caused the COVID-19 pandemic. Although passively delivered neutralizing antibodies against SARS-CoV-2 are in clinical trials, their mechanism of action in vivo is incompletely understood. Here, we define correlates of protection of neutralizing human monoclonal antibodies (mAbs) in SARS-CoV-2-infected mice. Whereas Fc effector functions are fully dispensable when mAbs are administered as prophylaxis, they are required for optimal protection as therapy. When given after infection, intact but not LALA-PG loss of Fc effector function variant mAbs reduce SARS-CoV-2 burden and lung disease in mice and hamsters. Fc engagement of neutralizing antibodies mitigates inflammation and improves respiratory mechanics, and transcriptional profiling suggests these phenotypes are associated with diminished innate immune signaling and enhanced tissue repair. Immune cell depletions establish that neutralizing mAbs require monocytes for therapeutic efficacy. Our study demonstrates that therapeutic neutralizing mAbs require Fc effector functions to reduce SARS-CoV-2 infection and modulate protective immune responses.

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