TocilizumabV1, PubMed, Checkpoint, bibRecord, 001151

Cutting edge: circulating plasmablasts induce the differentiation of human T follicular helper cells via IL-6 production.

Identifieur interne : 001151 ( PubMed/Checkpoint ); précédent : 001150; suivant : 001152

Cutting edge: circulating plasmablasts induce the differentiation of human T follicular helper cells via IL-6 production.

Auteurs : Konstantia-Maria Chavele [Royaume-Uni] ; Eve Merry [Royaume-Uni] ; Michael R. Ehrenstein [Royaume-Uni]

Source :

Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2015.

RBID : pubmed:25681343

Descripteurs français

English descriptors

KwdEn :
- Antibodies, Monoclonal, Humanized (immunology), Antibodies, Monoclonal, Humanized (therapeutic use), Antigens, CD19 (immunology), Antigens, CD19 (metabolism), Arthritis, Rheumatoid (blood), Arthritis, Rheumatoid (drug therapy), Arthritis, Rheumatoid (immunology), B-Lymphocytes (immunology), B-Lymphocytes (metabolism), CD4-Positive T-Lymphocytes (immunology), CD4-Positive T-Lymphocytes (metabolism), Cell Differentiation (immunology), Cell Proliferation, Cells, Cultured, Coculture Techniques, DNA-Binding Proteins (immunology), DNA-Binding Proteins (metabolism), Flow Cytometry, Humans, Inducible T-Cell Co-Stimulator Protein (immunology), Inducible T-Cell Co-Stimulator Protein (metabolism), Interleukin-6 (immunology), Interleukin-6 (metabolism), Interleukins (immunology), Interleukins (metabolism), Plasma Cells (immunology), Plasma Cells (metabolism), Proto-Oncogene Proteins c-bcl-6, Receptors, CXCR5 (immunology), Receptors, CXCR5 (metabolism), T-Lymphocytes, Helper-Inducer (immunology), T-Lymphocytes, Helper-Inducer (metabolism).
MESH :
- chemical , immunology : Antibodies, Monoclonal, Humanized, Antigens, CD19, DNA-Binding Proteins, Inducible T-Cell Co-Stimulator Protein, Interleukin-6, Interleukins, Receptors, CXCR5.
- chemical , metabolism : Antigens, CD19, DNA-Binding Proteins, Inducible T-Cell Co-Stimulator Protein, Interleukin-6, Interleukins, Receptors, CXCR5.
- chemical , therapeutic use : Antibodies, Monoclonal, Humanized.
- blood : Arthritis, Rheumatoid.
- drug therapy : Arthritis, Rheumatoid.
- immunology : Arthritis, Rheumatoid, B-Lymphocytes, CD4-Positive T-Lymphocytes, Cell Differentiation, Plasma Cells, T-Lymphocytes, Helper-Inducer.
- metabolism : B-Lymphocytes, CD4-Positive T-Lymphocytes, Plasma Cells, T-Lymphocytes, Helper-Inducer.
- Cell Proliferation, Cells, Cultured, Coculture Techniques, Flow Cytometry, Humans, Proto-Oncogene Proteins c-bcl-6.

Abstract

B cells require CD4(+) T follicular helper (Tfh) cells to progress through the germinal center and provide protective Ab responses. In this article, we reveal a reciprocal interaction whereby circulating human plasmablasts are potent inducers of the Tfh cell-differentiation program, including the expression of their key transcription factor Bcl-6. The markedly increased propensity of plasmablasts, compared with naive B cells, to induce Tfh cell differentiation was due to their increased production of IL-6. Specific targeting of IL-6 using tocilizumab therapy in patients with rheumatoid arthritis led to a significant reduction in circulating Tfh cell numbers and IL-21 production, which was correlated with reduced plasmablast formation. Our data uncover a positive-feedback loop between circulating plasmablasts and Tfh cells that could sustain autoimmunity and spread Ab-driven inflammation to unaffected sites; this represents an important therapeutic target, as well as reveals a novel mechanism of action for tocilizumab.

DOI: 10.4049/jimmunol.1401190
PubMed: 25681343

Affiliations:

Links toward previous steps (curation, corpus...)

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to stream PubMed, to step Curation: 001212

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pubmed:25681343

Le document en format XML

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<front><div type="abstract" xml:lang="en">B cells require CD4(+) T follicular helper (Tfh) cells to progress through the germinal center and provide protective Ab responses. In this article, we reveal a reciprocal interaction whereby circulating human plasmablasts are potent inducers of the Tfh cell-differentiation program, including the expression of their key transcription factor Bcl-6. The markedly increased propensity of plasmablasts, compared with naive B cells, to induce Tfh cell differentiation was due to their increased production of IL-6. Specific targeting of IL-6 using tocilizumab therapy in patients with rheumatoid arthritis led to a significant reduction in circulating Tfh cell numbers and IL-21 production, which was correlated with reduced plasmablast formation. Our data uncover a positive-feedback loop between circulating plasmablasts and Tfh cells that could sustain autoimmunity and spread Ab-driven inflammation to unaffected sites; this represents an important therapeutic target, as well as reveals a novel mechanism of action for tocilizumab. </div>
</front>
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<Abstract><AbstractText>B cells require CD4(+) T follicular helper (Tfh) cells to progress through the germinal center and provide protective Ab responses. In this article, we reveal a reciprocal interaction whereby circulating human plasmablasts are potent inducers of the Tfh cell-differentiation program, including the expression of their key transcription factor Bcl-6. The markedly increased propensity of plasmablasts, compared with naive B cells, to induce Tfh cell differentiation was due to their increased production of IL-6. Specific targeting of IL-6 using tocilizumab therapy in patients with rheumatoid arthritis led to a significant reduction in circulating Tfh cell numbers and IL-21 production, which was correlated with reduced plasmablast formation. Our data uncover a positive-feedback loop between circulating plasmablasts and Tfh cells that could sustain autoimmunity and spread Ab-driven inflammation to unaffected sites; this represents an important therapeutic target, as well as reveals a novel mechanism of action for tocilizumab. </AbstractText>
<CopyrightInformation>Copyright © 2015 The Authors.</CopyrightInformation>
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Cutting edge: circulating plasmablasts induce the differentiation of human T follicular helper cells via IL-6 production.

Cutting edge: circulating plasmablasts induce the differentiation of human T follicular helper cells via IL-6 production.

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