Secondary influenza challenge triggers resident memory B cell migration and rapid relocation to boost antibody secretion at infected sites

MacLean, Andrew J.; Richmond, Niamh; Koneva, Lada A.; Attar, Moustafa; Prada-Medina, César Augusto; Thornton, Emily; Gomes, Ariane; El-Turabi, Aadil; Bachmann, Martin F.; Rijal, Pramila; Tan, Tiong Kit; Townsend, Alain; Sansom, Stephen N.; Bannard, Oliver; Arnon, Tal I.

doi:10.1016/j.immuni.2022.03.003

Cited by 64 publications

(89 citation statements)

References 81 publications

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“…In the last few years, it became evident that the presence of MBCs is not restricted to secondary lymphoid organs. Infection with the influenza virus leads to the development of lung-resident MBCs, which persist in the lung mucosa for long periods of time ( Allie et al., 2019 ; MacLean et al., 2022 ; Oh et al., 2021 ; Tan et al., 2022 ). These studies identified MBCs based on their ability to bind fluorescently labeled flu proteins.…”

Section: Discussionmentioning

confidence: 99%

Viral infection engenders bona fide and bystander subsets of lung-resident memory B cells through a permissive mechanism

et al. 2022

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Section: Discussionmentioning

confidence: 99%

Viral infection engenders bona fide and bystander subsets of lung-resident memory B cells through a permissive mechanism

et al. 2022

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“…Recently, the fate of BRMs upon secondary challenge was reported ( 21 ). In a live-imaging analysis, alveolar BRMs of influenza-infected mice were attracted by CXCL9 and CXCL10 induced by alveolar macrophages and migrated to inflammation foci to differentiate into PCs upon secondary challenge.…”

Section: Tissue-resident Memory B Cellsmentioning

confidence: 99%

“…A recent study reported that BRMs not situated in the iBALTs, namely alveolar BRMs, relocate themselves to the inflammatory foci upon secondary challenge in an influenza virus infection model ( 21 ). In this study, aggregates of previously activated B cells within iBALT that express tdTomato in Aicda (AID) Cre/+ Rosa26 tdTomato reporter mice expressed the GC B-cell marker GL7 as well.…”

Section: Questions About Resident Memory B Cellsmentioning

confidence: 99%

Resident Memory B Cells in Barrier Tissues

Lee

2022

Front. Immunol.

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Epithelial barriers, which include the gastrointestinal, respiratory, and genitourinary mucosa, compose the body’s front line of defense. Since barrier tissues are persistently exposed to microbial challenges, a rapid response that can deal with diverse invading pathogens is crucial. Because B cells have been perceived as indirectly contributing to immune responses through antibody production, B cells functioning in the peripheral organs have been outside the scope of researchers. However, recent evidence supports the existence of tissue-resident memory B cells (BRMs) in the lungs. This population’s defensive response was stronger and faster than that of their circulating counterparts and could resist heterogeneous strains. With such traits, BRMs could be a promising target for vaccine design, but much about them remains to be revealed, including their locations, origin, specific markers, and the mechanisms of their establishment and maintenance. There is evidence for resident B cells in organs other than the lungs, suggesting that B cells are directly involved in the immune reactions of multiple non-lymphoid organs. This review summarizes the history of the discovery of BRMs and discusses important unresolved questions. Unique characteristics of humoral immunity that play an important role in the peripheral organs will be described briefly. Future research on B cells residing in non-lymphoid organs will provide new insights to help solve major problems regarding human health.

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“…Thus, our recently developed murine model as harnessed in the current work may not only serve as a valuable tool to profile and explore niches of CNS resident memory T cells, but also B cells with relevance to human neurological disease conditions. The formation and maintenance of resident memory B cells have been recently described in the lungs (Tan et al 2022; Allie et al 2019; Barker et al 2021), with certain populations demonstrating ASC phenotypes upon reactivation (MacLean et al 2022). Our observations that B cell populations persist in the CNS following aCD20 administration, suggests that at least a fraction of these cells may be tissue resident.…”

Section: Discussionmentioning

confidence: 99%

Persistent virus-specific and clonally expanded antibody secreting cells respond to induced self antigen in the CNS

Agrafiotis

Dizerens

Vincenti

et al. 2022

Preprint

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B cells contribute to the pathogenesis of both cellular- and humoral-mediated central nervous system (CNS) inflammatory diseases through a variety of mechanisms. In such conditions, B cells may enter the CNS parenchyma and contribute to local tissue destruction. It remains unexplored, however, how infection and autoimmunity drive transcriptional phenotypes, repertoire features, and antibody functionality. Here, we profiled B cells from the CNS of murine models of intracranial (i.c.) viral infections and autoimmunity. We identified a population of clonally expanded, antibody secreting cells (ASCs) that had undergone class-switch recombination and extensive somatic hypermutation following i.c. infection with attenuated lymphocytic choriomeningitis virus (rLCMV). Recombinant expression and characterisation of these antibodies revealed specificity to viral antigens (LCMV glycoprotein GP), correlating with ASC persistence in the brain weeks after resolved infection. Furthermore, these virus-specific ASCs upregulated proliferation and expansion programs in response to the conditional and transient induction of the LCMV GP as a neo-self antigen by astrocytes. This class-switched, clonally expanded, and mutated population persisted and was even more pronounced when peripheral B cells were depleted prior to autoantigen induction in the CNS. In contrast, the most expanded B cell clones in mice with persistent expression of LCMV GP in the CNS did not exhibit neo-self antigen specificity, potentially a consequence of local tolerance induction. Finally, a comparable population of clonally expanded, class-switched, proliferating ASCs was detected in the cerebrospinal fluid of multiple sclerosis patients. Taken together, our findings support the existence of B cells that populate the CNS and are capable of responding to locally encountered autoantigens.

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Secondary influenza challenge triggers resident memory B cell migration and rapid relocation to boost antibody secretion at infected sites

Cited by 64 publications

References 81 publications

Viral infection engenders bona fide and bystander subsets of lung-resident memory B cells through a permissive mechanism

Viral infection engenders bona fide and bystander subsets of lung-resident memory B cells through a permissive mechanism

Resident Memory B Cells in Barrier Tissues

Persistent virus-specific and clonally expanded antibody secreting cells respond to induced self antigen in the CNS

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