Regulation of pulmonary plasma cell responses during secondary infection with influenza virus

During secondary infection with influenza virus, plasma cells (PCs) develop within the lung, providing a local source of antibodies. However, the site and mechanisms that regulate this process are poorly defined. Here, we show that while circulating memory B cells entered the lung during rechallenge...

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Main Authors: Maclean, AJ, Bonifacio Lopes, J, Oram, S, Mohsen, M, Bachmann, M, Arnon, TI
Format: Journal article
Language:English
Published: Rockefeller University Press 2024
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author Maclean, AJ
Bonifacio Lopes, J
Oram, S
Mohsen, M
Bachmann, M
Arnon, TI
author_facet Maclean, AJ
Bonifacio Lopes, J
Oram, S
Mohsen, M
Bachmann, M
Arnon, TI
author_sort Maclean, AJ
collection OXFORD
description During secondary infection with influenza virus, plasma cells (PCs) develop within the lung, providing a local source of antibodies. However, the site and mechanisms that regulate this process are poorly defined. Here, we show that while circulating memory B cells entered the lung during rechallenge and were activated within inducible bronchus-associated lymphoid tissues (iBALTs), resident memory B (BRM) cells responded earlier, and their activation occurred in a different niche: directly near infected alveoli. This process required NK cells but was largely independent of CD4 and CD8 T cells. Innate stimuli induced by virus-like particles containing ssRNA triggered BRM cell differentiation in the absence of cognate antigen, suggesting a low threshold of activation. In contrast, expansion of PCs in iBALTs took longer to develop and was critically dependent on CD4 T cells. Our work demonstrates that spatially distinct mechanisms evolved to support pulmonary secondary PC responses, and it reveals a specialized function for BRM cells as guardians of the alveoli.
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spelling oxford-uuid:d90792b3-e2fd-4ae6-b53b-5c72ef66ab222024-06-07T11:21:59ZRegulation of pulmonary plasma cell responses during secondary infection with influenza virusJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:d90792b3-e2fd-4ae6-b53b-5c72ef66ab22EnglishSymplectic ElementsRockefeller University Press2024Maclean, AJBonifacio Lopes, JOram, SMohsen, MBachmann, MArnon, TIDuring secondary infection with influenza virus, plasma cells (PCs) develop within the lung, providing a local source of antibodies. However, the site and mechanisms that regulate this process are poorly defined. Here, we show that while circulating memory B cells entered the lung during rechallenge and were activated within inducible bronchus-associated lymphoid tissues (iBALTs), resident memory B (BRM) cells responded earlier, and their activation occurred in a different niche: directly near infected alveoli. This process required NK cells but was largely independent of CD4 and CD8 T cells. Innate stimuli induced by virus-like particles containing ssRNA triggered BRM cell differentiation in the absence of cognate antigen, suggesting a low threshold of activation. In contrast, expansion of PCs in iBALTs took longer to develop and was critically dependent on CD4 T cells. Our work demonstrates that spatially distinct mechanisms evolved to support pulmonary secondary PC responses, and it reveals a specialized function for BRM cells as guardians of the alveoli.
spellingShingle Maclean, AJ
Bonifacio Lopes, J
Oram, S
Mohsen, M
Bachmann, M
Arnon, TI
Regulation of pulmonary plasma cell responses during secondary infection with influenza virus
title Regulation of pulmonary plasma cell responses during secondary infection with influenza virus
title_full Regulation of pulmonary plasma cell responses during secondary infection with influenza virus
title_fullStr Regulation of pulmonary plasma cell responses during secondary infection with influenza virus
title_full_unstemmed Regulation of pulmonary plasma cell responses during secondary infection with influenza virus
title_short Regulation of pulmonary plasma cell responses during secondary infection with influenza virus
title_sort regulation of pulmonary plasma cell responses during secondary infection with influenza virus
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