2.50
Hdl Handle:
http://hdl.handle.net/10033/302163
Title:
B-1-cell subpopulations contribute differently to gut immunity.
Authors:
Roy, Bishnudeo; Agarwal, Shiwani; Brennecke, Anne-Margarete; Krey, Martina; Pabst, Oliver; Düber, Sandra; Weiss, Siegfried
Abstract:
In mice, B-1 (B1a/B1b) cells are mainly located in the peritoneal cavity. B-1 cells are well known for their role in the early stages of Ab-mediated immune responses against pathogenic invasion as well as for the production of natural IgM antibodies. Although such B cells have been claimed to give rise to intestinal plasma cells producing IgA, a clear role of B-1 cells in IgA production in the gut-associated tissues is still not defined. Here, we employed the transgenic L2 mouse model characterized by the lack of B-2 cells and presence of B-1 cells as major B-cell subpopulation. The oligoclonality of the Ab repertoire in this mouse allowed us to take typical B1a cell VH sequences as indicators of the presence of IgM-producing B-1a cells in Peyer's patches as well as in lamina propria. However, amongst the IgAVH sequences recovered from the same tissues, none of the sequences showed B1a-cell specificity. Interestingly, all IgAVH sequences derived from the lamina propria of L2 mice displayed extensive numbers of nucleotide exchanges, indicating somatic hypermutation, and affinity maturation. This suggests that the contribution of natural unmutated IgA by B-1a cells to intestinal immunity is negligible.
Affiliation:
Molecular Immunology, Helmholtz Centre for Infection Research (HZI), Braunschweig, Germany.
Citation:
B-1-cell subpopulations contribute differently to gut immunity. 2013, 43 (8):2023-32 Eur. J. Immunol.
Journal:
European journal of immunology
Issue Date:
Aug-2013
URI:
http://hdl.handle.net/10033/302163
DOI:
10.1002/eji.201243070
PubMed ID:
23677546
Type:
Article
Language:
en
ISSN:
1521-4141
Appears in Collections:
publications of the research group molecular Immunology (MOLI)

Full metadata record

DC FieldValue Language
dc.contributor.authorRoy, Bishnudeoen_GB
dc.contributor.authorAgarwal, Shiwanien_GB
dc.contributor.authorBrennecke, Anne-Margareteen_GB
dc.contributor.authorKrey, Martinaen_GB
dc.contributor.authorPabst, Oliveren_GB
dc.contributor.authorDüber, Sandraen_GB
dc.contributor.authorWeiss, Siegfrieden_GB
dc.date.accessioned2013-09-24T08:01:48Z-
dc.date.available2013-09-24T08:01:48Z-
dc.date.issued2013-08-
dc.identifier.citationB-1-cell subpopulations contribute differently to gut immunity. 2013, 43 (8):2023-32 Eur. J. Immunol.en_GB
dc.identifier.issn1521-4141-
dc.identifier.pmid23677546-
dc.identifier.doi10.1002/eji.201243070-
dc.identifier.urihttp://hdl.handle.net/10033/302163-
dc.description.abstractIn mice, B-1 (B1a/B1b) cells are mainly located in the peritoneal cavity. B-1 cells are well known for their role in the early stages of Ab-mediated immune responses against pathogenic invasion as well as for the production of natural IgM antibodies. Although such B cells have been claimed to give rise to intestinal plasma cells producing IgA, a clear role of B-1 cells in IgA production in the gut-associated tissues is still not defined. Here, we employed the transgenic L2 mouse model characterized by the lack of B-2 cells and presence of B-1 cells as major B-cell subpopulation. The oligoclonality of the Ab repertoire in this mouse allowed us to take typical B1a cell VH sequences as indicators of the presence of IgM-producing B-1a cells in Peyer's patches as well as in lamina propria. However, amongst the IgAVH sequences recovered from the same tissues, none of the sequences showed B1a-cell specificity. Interestingly, all IgAVH sequences derived from the lamina propria of L2 mice displayed extensive numbers of nucleotide exchanges, indicating somatic hypermutation, and affinity maturation. This suggests that the contribution of natural unmutated IgA by B-1a cells to intestinal immunity is negligible.en_GB
dc.language.isoenen
dc.rightsArchived with thanks to European journal of immunologyen_GB
dc.titleB-1-cell subpopulations contribute differently to gut immunity.en
dc.typeArticleen
dc.contributor.departmentMolecular Immunology, Helmholtz Centre for Infection Research (HZI), Braunschweig, Germany.en_GB
dc.identifier.journalEuropean journal of immunologyen_GB

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