Interferon-alpha triggers B cell effector 1 (Be1) commitment.

B-cells can contribute to the pathogenesis of autoimmune diseases not only through auto-antibody secretion but also via cytokine production. Therapeutic depletion of B-cells influences the functions and maintenance of various T-cell subsets. The mechanisms governing the functional heterogeneity of B...

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Autores principales:	Marie-Ghislaine de Goër de Herve, Deniz Durali, Bamory Dembele, Massimo Giuliani, Tu-Anh Tran, Bruno Azzarone, Pierre Eid, Marc Tardieu, Jean-François Delfraissy, Yassine Taoufik
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/5bec8b4cab8641468eb47618c778b1e3
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spelling	oai:doaj.org-article:5bec8b4cab8641468eb47618c778b1e32021-11-18T06:54:49ZInterferon-alpha triggers B cell effector 1 (Be1) commitment.1932-620310.1371/journal.pone.0019366https://doaj.org/article/5bec8b4cab8641468eb47618c778b1e32011-04-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21559410/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203B-cells can contribute to the pathogenesis of autoimmune diseases not only through auto-antibody secretion but also via cytokine production. Therapeutic depletion of B-cells influences the functions and maintenance of various T-cell subsets. The mechanisms governing the functional heterogeneity of B-cell subsets as cytokine-producing cells are poorly understood. B-cells can differentiate into two functionally polarized effectors, one (B-effector-1-cells) producing a Th-1-like cytokine pattern and the other (Be2) producing a Th-2-like pattern. IL-12 and IFN-γ play a key role in Be1 polarization, but the initial trigger of Be1 commitment is unclear. Type-I-interferons are produced early in the immune response and prime several processes involved in innate and adaptive responses. Here, we report that IFN-α triggers a signaling cascade in resting human naive B-cells, involving STAT4 and T-bet, two key IFN-γ gene imprinting factors. IFN-α primed naive B-cells for IFN-γ production and increased IFN-γ gene responsiveness to IL-12. IFN-γ continues this polarization by re-inducing T-bet and up-regulating IL-12Rβ2 expression. IFN-α and IFN-γ therefore pave the way for the action of IL-12. These results point to a coordinated action of IFN-α, IFN-γ and IL-12 in Be1 polarization of naive B-cells, and may provide new insights into the mechanisms by which type-I-interferons favor autoimmunity.Marie-Ghislaine de Goër de HerveDeniz DuraliBamory DembeleMassimo GiulianiTu-Anh TranBruno AzzaronePierre EidMarc TardieuJean-François DelfraissyYassine TaoufikPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 4, p e19366 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Marie-Ghislaine de Goër de Herve Deniz Durali Bamory Dembele Massimo Giuliani Tu-Anh Tran Bruno Azzarone Pierre Eid Marc Tardieu Jean-François Delfraissy Yassine Taoufik Interferon-alpha triggers B cell effector 1 (Be1) commitment.
description	B-cells can contribute to the pathogenesis of autoimmune diseases not only through auto-antibody secretion but also via cytokine production. Therapeutic depletion of B-cells influences the functions and maintenance of various T-cell subsets. The mechanisms governing the functional heterogeneity of B-cell subsets as cytokine-producing cells are poorly understood. B-cells can differentiate into two functionally polarized effectors, one (B-effector-1-cells) producing a Th-1-like cytokine pattern and the other (Be2) producing a Th-2-like pattern. IL-12 and IFN-γ play a key role in Be1 polarization, but the initial trigger of Be1 commitment is unclear. Type-I-interferons are produced early in the immune response and prime several processes involved in innate and adaptive responses. Here, we report that IFN-α triggers a signaling cascade in resting human naive B-cells, involving STAT4 and T-bet, two key IFN-γ gene imprinting factors. IFN-α primed naive B-cells for IFN-γ production and increased IFN-γ gene responsiveness to IL-12. IFN-γ continues this polarization by re-inducing T-bet and up-regulating IL-12Rβ2 expression. IFN-α and IFN-γ therefore pave the way for the action of IL-12. These results point to a coordinated action of IFN-α, IFN-γ and IL-12 in Be1 polarization of naive B-cells, and may provide new insights into the mechanisms by which type-I-interferons favor autoimmunity.
format	article
author	Marie-Ghislaine de Goër de Herve Deniz Durali Bamory Dembele Massimo Giuliani Tu-Anh Tran Bruno Azzarone Pierre Eid Marc Tardieu Jean-François Delfraissy Yassine Taoufik
author_facet	Marie-Ghislaine de Goër de Herve Deniz Durali Bamory Dembele Massimo Giuliani Tu-Anh Tran Bruno Azzarone Pierre Eid Marc Tardieu Jean-François Delfraissy Yassine Taoufik
author_sort	Marie-Ghislaine de Goër de Herve
title	Interferon-alpha triggers B cell effector 1 (Be1) commitment.
title_short	Interferon-alpha triggers B cell effector 1 (Be1) commitment.
title_full	Interferon-alpha triggers B cell effector 1 (Be1) commitment.
title_fullStr	Interferon-alpha triggers B cell effector 1 (Be1) commitment.
title_full_unstemmed	Interferon-alpha triggers B cell effector 1 (Be1) commitment.
title_sort	interferon-alpha triggers b cell effector 1 (be1) commitment.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/5bec8b4cab8641468eb47618c778b1e3
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Interferon-alpha triggers B cell effector 1 (Be1) commitment.

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