Marginating transitional B cells modulate neutrophils in the lung during inflammation and pneumonia.
Animals
Aspergillosis
/ microbiology
B-Lymphocytes
/ pathology
Capillaries
/ pathology
Cell Adhesion
Chemokine CXCL13
/ metabolism
Integrin alpha5
/ metabolism
Intravital Microscopy
Lipoxins
/ metabolism
Lung
/ blood supply
Mice, Mutant Strains
Neutrophils
/ pathology
Pneumonia
/ diagnostic imaging
Receptors, CXCR5
/ metabolism
Single-Cell Analysis
Journal
The Journal of experimental medicine
ISSN: 1540-9538
Titre abrégé: J Exp Med
Pays: United States
ID NLM: 2985109R
Informations de publication
Date de publication:
06 09 2021
06 09 2021
Historique:
received:
18
02
2021
revised:
04
06
2021
accepted:
06
07
2021
entrez:
27
7
2021
pubmed:
28
7
2021
medline:
25
11
2021
Statut:
ppublish
Résumé
Pulmonary innate immunity is required for host defense; however, excessive neutrophil inflammation can cause life-threatening acute lung injury. B lymphocytes can be regulatory, yet little is known about peripheral transitional IgM+ B cells in terms of regulatory properties. Using single-cell RNA sequencing, we discovered eight IgM+ B cell subsets with unique gene regulatory networks in the lung circulation dominated by transitional type 1 B and type 2 B (T2B) cells. Lung intravital confocal microscopy revealed that T2B cells marginate in the pulmonary capillaries via CD49e and require CXCL13 and CXCR5. During lung inflammation, marginated T2B cells dampened excessive neutrophil vascular inflammation via the specialized proresolving molecule lipoxin A4 (LXA4). Exogenous CXCL13 dampened excessive neutrophilic inflammation by increasing marginated B cells, and LXA4 recapitulated neutrophil regulation in B cell-deficient mice during inflammation and fungal pneumonia. Thus, the lung microvasculature is enriched in multiple IgM+ B cell subsets with marginating capillary T2B cells that dampen neutrophil responses.
Identifiants
pubmed: 34313733
pii: 212511
doi: 10.1084/jem.20210409
pmc: PMC8318832
pii:
doi:
Substances chimiques
CXCR5 protein, mouse
0
Chemokine CXCL13
0
Cxcl13 protein, mouse
0
Integrin alpha5
0
Lipoxins
0
Receptors, CXCR5
0
lipoxin A4
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Video-Audio Media
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : CIHR
ID : RS-342013
Pays : Canada
Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2021 Podstawka et al.
Déclaration de conflit d'intérêts
Disclosures: The authors declare no competing interests exist.
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