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Memory B cells in the lung participate in protective humoral immune responses to pulmonary influenza virus reinfection.

ABSTRACT: After pulmonary virus infection, virus-binding B cells ectopically accumulate in the lung. However, their contribution to protective immunity against reinfecting viruses remains unknown. Here, we show the phenotypes and protective functions of virus-binding memory B cells that persist in the lung following pulmonary infection with influenza virus. A fraction of virus-binding B-cell population in the lung expressed surface markers for splenic mature memory B cells (CD73, CD80, and CD273) along with CD69 and CXCR3 that are up-regulated on lung effector/memory T cells. The lung B-cell population with memory phenotype persisted for more than 5 mo after infection, and on reinfection promptly differentiated into plasma cells that produced virus-neutralizing antibodies locally. This production of local IgG and IgA neutralizing antibody was correlated with reduced virus spread in adapted hosts. Our data demonstrates that infected lungs harbor a memory B-cell subset with distinctive phenotype and ability to provide protection against pulmonary virus reinfection.

SUBMITTER: Onodera T

PROVIDER: S-EPMC3289300 | biostudies-literature | 2012 Feb

REPOSITORIES: biostudies-literature

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Memory B cells in the lung participate in protective humoral immune responses to pulmonary influenza virus reinfection.

Onodera Taishi T Takahashi Yoshimasa Y Yokoi Yusuke Y Ato Manabu M Kodama Yuichi Y Hachimura Satoshi S Kurosaki Tomohiro T Kobayashi Kazuo K

Proceedings of the National Academy of Sciences of the United States of America 20120130 7

After pulmonary virus infection, virus-binding B cells ectopically accumulate in the lung. However, their contribution to protective immunity against reinfecting viruses remains unknown. Here, we show the phenotypes and protective functions of virus-binding memory B cells that persist in the lung following pulmonary infection with influenza virus. A fraction of virus-binding B-cell population in the lung expressed surface markers for splenic mature memory B cells (CD73, CD80, and CD273) along wi ...[more]

PMID: 22308386

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Project description:BackgroundResident phenotypic memory CD8+ T cells are crucial for immune defense against pathogens. However, little is known about the potential transitions and regulation mechanisms of their function after influenza virus infection and reinfection. In this study, we utilized integrated transcriptome data and in vivo experiments to investigate the key characteristics behind it.MethodsTwo single-cell RNA sequencing (scRNA-seq) datasets of lung CD8+ T cells and one RNA-seq dataset of lung tissue after infection or reinfection were included. After Seurat procedures classifying CD8+ T subsets, the scCODE algorithm was used to identify the differentially expressed genes for GSVA, GO, and KEGG pathway enrichment. Monocle 3 and CellChat were used to infer pseudotime cell trajectory and cell interactions. The ssGSEA method was used to estimate the relative proportions of immune cells. The findings were confirmed with a mouse model via flow cytometry and RT-PCR analysis.ResultsOur study refined the landscape of CD8+ T-cell subsets in the lung, showing that CD8+ Trm cells accumulated in the lung within 14 days after influenza infection. The classical CD8+ Trm cells co-expressed a high level of CD49a and even maintained 90 days after primary infection. The ratio of CD8+ Trm cells decreased 1 day after influenza reinfection, which may be parallel with their potential transition into effector types, as observed in trajectory inference analysis. KEGG analysis suggested that PD-L1 expression and PD-1 checkpoint pathway were upregulated in CD8+ Trm cells on day 14 after infection. GO and GSVA analyses revealed that PI3K-Akt-mTOR and type I interferon signaling pathways were enriched in CD8+ Tem and Trm cells after reinfection. Additionally, CCL signaling pathways were involved in cell interaction between CD8+ Trm cells and other cells, with Ccl4-Ccr5 and Ccl5-Ccr5 ligand/receptor pairs being important between CD8+ Trm and other memory subsets after infection and reinfection.ConclusionOur data suggest that resident memory CD8+ T cells with CD49a co-expression account for a large proportion after influenza infection, and they can be rapidly reactivated against reinfection. Function differences exist in CD8+ Trm and Tem cells after influenza infection and reinfection. Ccl5-Ccr5 ligand/receptor pair is important in cell interactions between CD8+ Trm and other subsets.

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Memory B cells in the lung participate in protective humoral immune responses to pulmonary influenza virus reinfection.

Publications

Memory B cells in the lung participate in protective humoral immune responses to pulmonary influenza virus reinfection.

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