Secondary influenza challenge triggers resident memory B cell migration and rapid relocation to boost antibody secretion at infected sites
Resident memory B (BRM) cells develop and persist in the lungs of influenza-infected mice and humans; however, their contribution to recall responses has not been defined. Here, we used two-photon microscopy to visualize BRM cells within the lungs of influenza -virus immune and reinfected mice. Prio...
Main Authors: | , , , , , , , , , , , , , , |
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Format: | Journal article |
Language: | English |
Published: |
Elsevier
2022
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_version_ | 1797107247860416512 |
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author | MacLean, AJ Richmond, N Koneva, L Attar, M Medina, CAP Thornton, EE Gomes, AC El-Turabi, A Bachmann, MF Rijal, P Tan, TK Townsend, A Sansom, SN Bannard, O Arnon, TI |
author_facet | MacLean, AJ Richmond, N Koneva, L Attar, M Medina, CAP Thornton, EE Gomes, AC El-Turabi, A Bachmann, MF Rijal, P Tan, TK Townsend, A Sansom, SN Bannard, O Arnon, TI |
author_sort | MacLean, AJ |
collection | OXFORD |
description | Resident memory B (BRM) cells develop and persist in the lungs of influenza-infected mice and humans; however, their contribution to recall responses has not been defined. Here, we used two-photon microscopy to visualize BRM cells within the lungs of influenza -virus immune and reinfected mice. Prior to re-exposure, BRM cells were sparsely scattered throughout the tissue, displaying limited motility. Within 24 h of rechallenge, these cells increased their migratory capacity, localized to infected sites, and subsequently differentiated into plasma cells. Alveolar macrophages mediated this process, in part by inducing expression of chemokines CXCL9 and CXCL10 from infiltrating inflammatory cells. This led to the recruitment of chemokine receptor CXCR3-expressing BRM cells to infected regions and increased local antibody concentrations. Our study uncovers spatiotemporal mechanisms that regulate lung BRM cell reactivation and demonstrates their capacity to rapidly deliver antibodies in a highly localized manner to sites of viral replication. |
first_indexed | 2024-03-07T07:11:50Z |
format | Journal article |
id | oxford-uuid:20151884-5728-4460-a25d-3cd59daa1167 |
institution | University of Oxford |
language | English |
last_indexed | 2024-03-07T07:11:50Z |
publishDate | 2022 |
publisher | Elsevier |
record_format | dspace |
spelling | oxford-uuid:20151884-5728-4460-a25d-3cd59daa11672022-07-13T09:06:02ZSecondary influenza challenge triggers resident memory B cell migration and rapid relocation to boost antibody secretion at infected sitesJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:20151884-5728-4460-a25d-3cd59daa1167EnglishSymplectic ElementsElsevier2022MacLean, AJRichmond, NKoneva, LAttar, MMedina, CAPThornton, EEGomes, ACEl-Turabi, ABachmann, MFRijal, PTan, TKTownsend, ASansom, SNBannard, OArnon, TIResident memory B (BRM) cells develop and persist in the lungs of influenza-infected mice and humans; however, their contribution to recall responses has not been defined. Here, we used two-photon microscopy to visualize BRM cells within the lungs of influenza -virus immune and reinfected mice. Prior to re-exposure, BRM cells were sparsely scattered throughout the tissue, displaying limited motility. Within 24 h of rechallenge, these cells increased their migratory capacity, localized to infected sites, and subsequently differentiated into plasma cells. Alveolar macrophages mediated this process, in part by inducing expression of chemokines CXCL9 and CXCL10 from infiltrating inflammatory cells. This led to the recruitment of chemokine receptor CXCR3-expressing BRM cells to infected regions and increased local antibody concentrations. Our study uncovers spatiotemporal mechanisms that regulate lung BRM cell reactivation and demonstrates their capacity to rapidly deliver antibodies in a highly localized manner to sites of viral replication. |
spellingShingle | MacLean, AJ Richmond, N Koneva, L Attar, M Medina, CAP Thornton, EE Gomes, AC El-Turabi, A Bachmann, MF Rijal, P Tan, TK Townsend, A Sansom, SN Bannard, O Arnon, TI Secondary influenza challenge triggers resident memory B cell migration and rapid relocation to boost antibody secretion at infected sites |
title | Secondary influenza challenge triggers resident memory B cell migration and rapid relocation to boost antibody secretion at infected sites |
title_full | Secondary influenza challenge triggers resident memory B cell migration and rapid relocation to boost antibody secretion at infected sites |
title_fullStr | Secondary influenza challenge triggers resident memory B cell migration and rapid relocation to boost antibody secretion at infected sites |
title_full_unstemmed | Secondary influenza challenge triggers resident memory B cell migration and rapid relocation to boost antibody secretion at infected sites |
title_short | Secondary influenza challenge triggers resident memory B cell migration and rapid relocation to boost antibody secretion at infected sites |
title_sort | secondary influenza challenge triggers resident memory b cell migration and rapid relocation to boost antibody secretion at infected sites |
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