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Oral-Nasopharyngeal Dendritic Cells Mediate T Cell-Independent IgA Class Switching on B-1 B Cells

Native cholera toxin (nCT) as a nasal adjuvant was shown to elicit increased levels of T-independent S-IgA antibody (Ab) responses through IL-5- IL-5 receptor interactions between CD4(+) T cells and IgA(+) B-1 B cells in murine submandibular glands (SMGs) and nasal passages (NPs). Here, we further i...

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Autores principales: Kataoka, Kosuke, Fujihashi, Keiko, Terao, Yutaka, Gilbert, Rebekah S., Sekine, Shinichi, Kobayashi, Ryoki, Fukuyama, Yoshiko, Kawabata, Shigetada, Fujihashi, Kohtaro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183055/
https://www.ncbi.nlm.nih.gov/pubmed/21980444
http://dx.doi.org/10.1371/journal.pone.0025396
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author Kataoka, Kosuke
Fujihashi, Keiko
Terao, Yutaka
Gilbert, Rebekah S.
Sekine, Shinichi
Kobayashi, Ryoki
Fukuyama, Yoshiko
Kawabata, Shigetada
Fujihashi, Kohtaro
author_facet Kataoka, Kosuke
Fujihashi, Keiko
Terao, Yutaka
Gilbert, Rebekah S.
Sekine, Shinichi
Kobayashi, Ryoki
Fukuyama, Yoshiko
Kawabata, Shigetada
Fujihashi, Kohtaro
author_sort Kataoka, Kosuke
collection PubMed
description Native cholera toxin (nCT) as a nasal adjuvant was shown to elicit increased levels of T-independent S-IgA antibody (Ab) responses through IL-5- IL-5 receptor interactions between CD4(+) T cells and IgA(+) B-1 B cells in murine submandibular glands (SMGs) and nasal passages (NPs). Here, we further investigate whether oral-nasopharyngeal dendritic cells (DCs) play a central role in the induction of B-1 B cell IgA class switch recombination (CSR) for the enhancement of T cell-independent (TI) mucosal S-IgA Ab responses. High expression levels of activation-induced cytidine deaminase, Iα-Cμ circulation transcripts and Iμ-Cα transcripts were seen on B-1 B cells purified from SMGs and NPs of both TCRβ(−/−) mice and wild-type mice given nasal trinitrophenyl (TNP)-LPS plus nCT, than in the same tissues of mice given nCT or TNP-LPS alone. Further, DCs from SMGs, NPs and NALT of mice given nasal TNP-LPS plus nCT expressed significantly higher levels of a proliferation-inducing ligand (APRIL) than those in mice given TNP-LPS or nCT alone, whereas the B-1 B cells in SMGs and NPs showed elevated levels of transmembrane activator and calcium modulator cyclophilin ligand interactor (TACI) expression. Interestingly, high frequencies of IgA(+) B-1 B cells were induced when peritoneal IgA(−) IgM(+) B cells were stimulated with mucosal DCs from mice given nasal TNP-LPS plus nCT. Taken together, these findings show that nasal nCT plays a key role in the enhancement of mucosal DC-mediated TI IgA CSR by B-1 B cells through their interactions with APRIL and TACI.
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spelling pubmed-31830552011-10-06 Oral-Nasopharyngeal Dendritic Cells Mediate T Cell-Independent IgA Class Switching on B-1 B Cells Kataoka, Kosuke Fujihashi, Keiko Terao, Yutaka Gilbert, Rebekah S. Sekine, Shinichi Kobayashi, Ryoki Fukuyama, Yoshiko Kawabata, Shigetada Fujihashi, Kohtaro PLoS One Research Article Native cholera toxin (nCT) as a nasal adjuvant was shown to elicit increased levels of T-independent S-IgA antibody (Ab) responses through IL-5- IL-5 receptor interactions between CD4(+) T cells and IgA(+) B-1 B cells in murine submandibular glands (SMGs) and nasal passages (NPs). Here, we further investigate whether oral-nasopharyngeal dendritic cells (DCs) play a central role in the induction of B-1 B cell IgA class switch recombination (CSR) for the enhancement of T cell-independent (TI) mucosal S-IgA Ab responses. High expression levels of activation-induced cytidine deaminase, Iα-Cμ circulation transcripts and Iμ-Cα transcripts were seen on B-1 B cells purified from SMGs and NPs of both TCRβ(−/−) mice and wild-type mice given nasal trinitrophenyl (TNP)-LPS plus nCT, than in the same tissues of mice given nCT or TNP-LPS alone. Further, DCs from SMGs, NPs and NALT of mice given nasal TNP-LPS plus nCT expressed significantly higher levels of a proliferation-inducing ligand (APRIL) than those in mice given TNP-LPS or nCT alone, whereas the B-1 B cells in SMGs and NPs showed elevated levels of transmembrane activator and calcium modulator cyclophilin ligand interactor (TACI) expression. Interestingly, high frequencies of IgA(+) B-1 B cells were induced when peritoneal IgA(−) IgM(+) B cells were stimulated with mucosal DCs from mice given nasal TNP-LPS plus nCT. Taken together, these findings show that nasal nCT plays a key role in the enhancement of mucosal DC-mediated TI IgA CSR by B-1 B cells through their interactions with APRIL and TACI. Public Library of Science 2011-09-29 /pmc/articles/PMC3183055/ /pubmed/21980444 http://dx.doi.org/10.1371/journal.pone.0025396 Text en Kataoka et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Kataoka, Kosuke
Fujihashi, Keiko
Terao, Yutaka
Gilbert, Rebekah S.
Sekine, Shinichi
Kobayashi, Ryoki
Fukuyama, Yoshiko
Kawabata, Shigetada
Fujihashi, Kohtaro
Oral-Nasopharyngeal Dendritic Cells Mediate T Cell-Independent IgA Class Switching on B-1 B Cells
title Oral-Nasopharyngeal Dendritic Cells Mediate T Cell-Independent IgA Class Switching on B-1 B Cells
title_full Oral-Nasopharyngeal Dendritic Cells Mediate T Cell-Independent IgA Class Switching on B-1 B Cells
title_fullStr Oral-Nasopharyngeal Dendritic Cells Mediate T Cell-Independent IgA Class Switching on B-1 B Cells
title_full_unstemmed Oral-Nasopharyngeal Dendritic Cells Mediate T Cell-Independent IgA Class Switching on B-1 B Cells
title_short Oral-Nasopharyngeal Dendritic Cells Mediate T Cell-Independent IgA Class Switching on B-1 B Cells
title_sort oral-nasopharyngeal dendritic cells mediate t cell-independent iga class switching on b-1 b cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183055/
https://www.ncbi.nlm.nih.gov/pubmed/21980444
http://dx.doi.org/10.1371/journal.pone.0025396
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