Bacterial lectin BambL acts as a B cell superantigen.
Adaptive immunity
Apoptosis
Bacterial pathogens
Immunoglobulin glycosylation
Multivalent lectins
β-Propeller lectins
Journal
Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402
Informations de publication
Date de publication:
Dec 2021
Dec 2021
Historique:
received:
23
12
2020
accepted:
21
10
2021
revised:
03
10
2021
pubmed:
4
11
2021
medline:
15
12
2021
entrez:
3
11
2021
Statut:
ppublish
Résumé
B cell superantigens crosslink conserved domains of B cell receptors (BCRs) and cause dysregulated, polyclonal B cell activation irrespective of normal BCR-antigen complementarity. The cells typically succumb to activation-induced cell death, which can impede the adaptive immune response and favor infection. In the present study, we demonstrate that the fucose-binding lectin of Burkholderia ambifaria, BambL, bears functional resemblance to B cell superantigens. By engaging surface glycans, the bacterial lectin activated human peripheral blood B cells, which manifested in the surface expression of CD69, CD54 and CD86 but became increasingly cytotoxic at higher concentrations. The effects were sensitive to BCR pathway inhibitors and excess fucose, which corroborates a glycan-driven mode of action. Interactome analyses in a model cell line suggest BambL binds directly to glycans of the BCR and regulatory coreceptors. In vitro, BambL triggered BCR signaling and induced CD19 internalization and degradation. Owing to the lectin's six binding sites, we propose a BCR activation model in which BambL functions as a clustering hub for receptor glycans, modulates normal BCR regulation, and induces cell death through exhaustive activation.
Identifiants
pubmed: 34731252
doi: 10.1007/s00018-021-04009-z
pii: 10.1007/s00018-021-04009-z
pmc: PMC8629787
doi:
Substances chimiques
Bacterial Proteins
0
Lectins
0
Polysaccharides
0
Receptors, Antigen, B-Cell
0
Superantigens
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
8165-8186Subventions
Organisme : Max-Planck-Gesellschaft
ID : IMPRS-MCB
Organisme : Deutsche Forschungsgemeinschaft
ID : RTG-2202
Organisme : Deutsche Forschungsgemeinschaft
ID : EXC-294
Organisme : Deutsche Forschungsgemeinschaft
ID : GSC-4
Organisme : Ministerium für Wissenschaft, Forschung und Kunst Baden-Württemberg
ID : Az: 33 7532.20
Informations de copyright
© 2021. The Author(s).
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