tetano
Editor, Senior Moderator
J Exp Med
. 2024 Jul 1;221(7):e20232014.
doi: 10.1084/jem.20232014. Epub 2024 Apr 25. Regulation of pulmonary plasma cell responses during secondary infection with influenza virus
Andrew J MacLean[SUP] 1 [/SUP], Joao P P L Bonifacio[SUP] 1 [/SUP], Sophia L Oram[SUP] 1 [/SUP], Mona O Mohsen[SUP] 2 [/SUP], Martin F Bachmann[SUP] 3 2 [/SUP], Tal I Arnon[SUP] 1 [/SUP]
Affiliations
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.
. 2024 Jul 1;221(7):e20232014.
doi: 10.1084/jem.20232014. Epub 2024 Apr 25. Regulation of pulmonary plasma cell responses during secondary infection with influenza virus
Andrew J MacLean[SUP] 1 [/SUP], Joao P P L Bonifacio[SUP] 1 [/SUP], Sophia L Oram[SUP] 1 [/SUP], Mona O Mohsen[SUP] 2 [/SUP], Martin F Bachmann[SUP] 3 2 [/SUP], Tal I Arnon[SUP] 1 [/SUP]
Affiliations
- PMID: 38661717
- PMCID: PMC11044945
- DOI: 10.1084/jem.20232014
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.