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Gut microbiota influence B cell function in a TLR5-dependent manner

Sha Li, William Walters, Benoit Chassaing, Benyue Zhang, Qiaojuan Shi, Jillian Waters, Andrew T. Gewirtz, Cynthia A. Leifer, Ruth Ley
doi: https://doi.org/10.1101/537894
Sha Li
1 Department of Microbiology, Department of Molecular Biology and Genetics, Cornell University;
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William Walters
2 Department of Microbiome Science, Max Planck Institute for Developmental Biology;
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  • For correspondence: william.a.walters@gmail.com
Benoit Chassaing
3 Neuroscience Institute, Georgia State University,Institute of Biomedical Sciences,Georgia State Univ;
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Benyue Zhang
4 Institute of Biomedical Sciences, Georgia State University;
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Qiaojuan Shi
1 Department of Microbiology, Department of Molecular Biology and Genetics, Cornell University;
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Jillian Waters
2 Department of Microbiome Science, Max Planck Institute for Developmental Biology;
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Andrew T. Gewirtz
4 Institute of Biomedical Sciences, Georgia State University;
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Cynthia A. Leifer
5 Department of Microbiology and Immunology, Cornell University
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Ruth Ley
2 Department of Microbiome Science, Max Planck Institute for Developmental Biology;
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  • For correspondence: ruth.ley@tuebingen.mpg.de
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Abstract

Toll-like receptor (TLR) 5-deficient mice display aberrantly low levels of flagellin-specific antibodies (Flic-IgA) secreted into the gut, combined with excess bacterial flagellin in the gut, and together these attributes define microbiome dysbiosis (T5-dysbiosis). How TLR5 signaling deficiency results in T5-dysbiosis is unclear. Here, we address the role of B cells in T-dysbiosis. We observed that B cells do not express TLR5, and that B cell transplantation from TLR5-/- mouse donors into B-cell deficient mice resulted in a slight reduction in Flic-IgA levels compared to B-cells from WT donors. Bone marrow transplants from WT and TLR5-/- donors into recipients of both genotypes confirmed that TLR5 signaling by non-hematopoietic cells is required for T5-dysbiosis. We observed TLR5 deficiency was associated with an expanded population of IgA+ B cells. TLR5-/- mice tended to have higher richness for the IgA gene hypervariable region (CDR3 gene) variants. Transplantation of microbiomes from TLR5-/- and WT microbiomes donors into germfree mice resulted in a higher proportion of IgA-secreting B cells, and higher overall fecal IgA and anti-Flic IgA for TLR5-/- microbiome recipients. This observation indicated that the TLR5-/- mouse microbiome elicits an anti-flagellin antibody response that requires TLR5 signaling. Together these results indicate that TLR5 signaling on epithelial cells influences B cell populations and antibody repertoire.

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  • Incorrect author order entered initially

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Posted February 07, 2019.
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Gut microbiota influence B cell function in a TLR5-dependent manner
Sha Li, William Walters, Benoit Chassaing, Benyue Zhang, Qiaojuan Shi, Jillian Waters, Andrew T. Gewirtz, Cynthia A. Leifer, Ruth Ley
bioRxiv 537894; doi: https://doi.org/10.1101/537894
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Gut microbiota influence B cell function in a TLR5-dependent manner
Sha Li, William Walters, Benoit Chassaing, Benyue Zhang, Qiaojuan Shi, Jillian Waters, Andrew T. Gewirtz, Cynthia A. Leifer, Ruth Ley
bioRxiv 537894; doi: https://doi.org/10.1101/537894

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