The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88

Bing He; Raul Santamaria; Weifeng Xu; Montserrat Cols; Kang Chen; Irene Puga; Meimei Shan; Huabao Xiong; James B. Bussel; April Chiu; Anne Puel; Jeanine Reichenbach; László Marodi; Rainer Döffinger; Julia Vasconcelos; Andrew Issekutz; Jens Krause; Graham Davies; Xiaoxia Li; Bodo Grimbacher; Alessandro Plebani; Eric Meffre; Capucine Picard; Charlotte Cunningham-Rundles; Jean Laurent Casanova; Andrea Cerutti

doi:10.1038/ni.1914

The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88

Bing He, Raul Santamaria, Weifeng Xu, Montserrat Cols, Kang Chen, Irene Puga, Meimei Shan, Huabao Xiong, James B. Bussel, April Chiu, Anne Puel, Jeanine Reichenbach, László Marodi, Rainer Döffinger, Julia Vasconcelos, Andrew Issekutz, Jens Krause, Graham Davies, Xiaoxia Li, Bodo GrimbacherAlessandro Plebani, Eric Meffre, Capucine Picard, Charlotte Cunningham-Rundles, Jean Laurent Casanova, Andrea Cerutti

Résultat de recherche: Article › examen par les pairs

284 Citations (Scopus)

Résumé

BAFF and APRIL are innate immune mediators that trigger immunoglobulin G (IgG) and IgA class-switch recombination (CSR) in B cells by engaging the receptor TACI. The mechanism that underlies CSR signaling by TACI remains unknown. Here we found that the cytoplasmic domain of TACI encompasses a conserved motif that bound MyD88, an adaptor that activates transcription factor NF-κB signaling pathways via a Toll-interleukin 1 (IL-1) receptor (TIR) domain. TACI lacks a TIR domain, yet triggered CSR via the DNA-editing enzyme AID by activating NF-κB through a Toll-like receptor (TLR)-like MyD88-IRAK1-IRAK4-TRAF6-TAK1 pathway. TACI-induced CSR was impaired in mice and humans lacking MyD88 or the kinase IRAK4, which indicates that MyD88 controls a B cell-intrinsic, TIR-independent, TACI-dependent pathway for immunoglobulin diversification.

Langue d'origine	English
Pages (de-à)	836-845
Nombre de pages	10
Journal	Nature Immunology
Volume	11
Numéro de publication	9
DOI	https://doi.org/10.1038/ni.1914
Statut de publication	Published - sept. 2010
Publié à l'externe	Oui

Note bibliographique

Funding Information:
We thank S.Y. Zhang (University Paris Descartes) for peripheral blood mononuclear cells from patients deficient in the transmembrane protein Unc93b; S. Vogel and A. Medvedev (University of Maryland) for DN-IRAK4-C877T; J.D. Li (University of South California) for DN-IKKα(K44M) and DN-IKKβ(K49A); J. Jun Ninomiya-Tsuji (Lerner Research Institute) for DN-TAK1(K63W); Z. Cao (Tularik) for DN-IRAK1 (1–208); and the Mount Sinai School of Medicine Microscopy Shared Resource Facility. Supported by the US National Institutes of Health (R01 AI-05753 and R01 AI-074378 to A. Cerutti and S10RR09145), Catalan Institute for Research and Advanced Studies (A. Cerutti), Fundacio’ Institut Municipal d’Investigació Mèdica (A. Cerutti), Ministerio de Ciencia e Innovación (SAF 2008-02725 to A. Cerutti), The Irma T. Hirschl Charitable Trust (A. Cerutti), Comissionat per a Universitats i Recerca del Departament d’Innovació, Universitats i Empresa de la Generalitat de Catalunya (R.S.), Programa Juán de la Cierva (I.P.), Fondazione C. Golgi and Centro Immunodeficienze Mario di Martino (A. Plebani), TÁMOP (4.2.2-08/1-2008-0015 to L.M.), the US National Institutes of Health–National Cancer Institute (5R24 CA095823) and the National Science Foundation (DBI-9724504).

ASJC Scopus Subject Areas

Immunology and Allergy
Immunology

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10.1038/ni.1914

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He, B., Santamaria, R., Xu, W., Cols, M., Chen, K., Puga, I., Shan, M., Xiong, H., Bussel, J. B., Chiu, A., Puel, A., Reichenbach, J., Marodi, L., Döffinger, R., Vasconcelos, J., Issekutz, A., Krause, J., Davies, G., Li, X., ... Cerutti, A. (2010). The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88. Nature Immunology, 11(9), 836-845. https://doi.org/10.1038/ni.1914

He, B, Santamaria, R, Xu, W, Cols, M, Chen, K, Puga, I, Shan, M, Xiong, H, Bussel, JB, Chiu, A, Puel, A, Reichenbach, J, Marodi, L, Döffinger, R, Vasconcelos, J, Issekutz, A, Krause, J, Davies, G, Li, X, Grimbacher, B, Plebani, A, Meffre, E, Picard, C, Cunningham-Rundles, C, Casanova, JL & Cerutti, A 2010, 'The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88', Nature Immunology, vol. 11, n° 9, pp. 836-845. https://doi.org/10.1038/ni.1914

@article{fc25fbd3224341b399b50daa07af6bab,

title = "The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88",

abstract = "BAFF and APRIL are innate immune mediators that trigger immunoglobulin G (IgG) and IgA class-switch recombination (CSR) in B cells by engaging the receptor TACI. The mechanism that underlies CSR signaling by TACI remains unknown. Here we found that the cytoplasmic domain of TACI encompasses a conserved motif that bound MyD88, an adaptor that activates transcription factor NF-κB signaling pathways via a Toll-interleukin 1 (IL-1) receptor (TIR) domain. TACI lacks a TIR domain, yet triggered CSR via the DNA-editing enzyme AID by activating NF-κB through a Toll-like receptor (TLR)-like MyD88-IRAK1-IRAK4-TRAF6-TAK1 pathway. TACI-induced CSR was impaired in mice and humans lacking MyD88 or the kinase IRAK4, which indicates that MyD88 controls a B cell-intrinsic, TIR-independent, TACI-dependent pathway for immunoglobulin diversification.",

author = "Bing He and Raul Santamaria and Weifeng Xu and Montserrat Cols and Kang Chen and Irene Puga and Meimei Shan and Huabao Xiong and Bussel, {James B.} and April Chiu and Anne Puel and Jeanine Reichenbach and L{\'a}szl{\'o} Marodi and Rainer D{\"o}ffinger and Julia Vasconcelos and Andrew Issekutz and Jens Krause and Graham Davies and Xiaoxia Li and Bodo Grimbacher and Alessandro Plebani and Eric Meffre and Capucine Picard and Charlotte Cunningham-Rundles and Casanova, {Jean Laurent} and Andrea Cerutti",

note = "Funding Information: We thank S.Y. Zhang (University Paris Descartes) for peripheral blood mononuclear cells from patients deficient in the transmembrane protein Unc93b; S. Vogel and A. Medvedev (University of Maryland) for DN-IRAK4-C877T; J.D. Li (University of South California) for DN-IKKα(K44M) and DN-IKKβ(K49A); J. Jun Ninomiya-Tsuji (Lerner Research Institute) for DN-TAK1(K63W); Z. Cao (Tularik) for DN-IRAK1 (1–208); and the Mount Sinai School of Medicine Microscopy Shared Resource Facility. Supported by the US National Institutes of Health (R01 AI-05753 and R01 AI-074378 to A. Cerutti and S10RR09145), Catalan Institute for Research and Advanced Studies (A. Cerutti), Fundacio{\textquoteright} Institut Municipal d{\textquoteright}Investigaci{\'o} M{\`e}dica (A. Cerutti), Ministerio de Ciencia e Innovaci{\'o}n (SAF 2008-02725 to A. Cerutti), The Irma T. Hirschl Charitable Trust (A. Cerutti), Comissionat per a Universitats i Recerca del Departament d{\textquoteright}Innovaci{\'o}, Universitats i Empresa de la Generalitat de Catalunya (R.S.), Programa Ju{\'a}n de la Cierva (I.P.), Fondazione C. Golgi and Centro Immunodeficienze Mario di Martino (A. Plebani), T{\'A}MOP (4.2.2-08/1-2008-0015 to L.M.), the US National Institutes of Health–National Cancer Institute (5R24 CA095823) and the National Science Foundation (DBI-9724504).",

year = "2010",

month = sep,

doi = "10.1038/ni.1914",

language = "English",

volume = "11",

pages = "836--845",

journal = "Nature Immunology",

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T1 - The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88

AU - He, Bing

AU - Santamaria, Raul

AU - Xu, Weifeng

AU - Cols, Montserrat

AU - Chen, Kang

AU - Puga, Irene

AU - Shan, Meimei

AU - Xiong, Huabao

AU - Bussel, James B.

AU - Chiu, April

AU - Puel, Anne

AU - Reichenbach, Jeanine

AU - Marodi, László

AU - Döffinger, Rainer

AU - Vasconcelos, Julia

AU - Issekutz, Andrew

AU - Krause, Jens

AU - Davies, Graham

AU - Li, Xiaoxia

AU - Grimbacher, Bodo

AU - Plebani, Alessandro

AU - Meffre, Eric

AU - Picard, Capucine

AU - Cunningham-Rundles, Charlotte

AU - Casanova, Jean Laurent

AU - Cerutti, Andrea

N1 - Funding Information: We thank S.Y. Zhang (University Paris Descartes) for peripheral blood mononuclear cells from patients deficient in the transmembrane protein Unc93b; S. Vogel and A. Medvedev (University of Maryland) for DN-IRAK4-C877T; J.D. Li (University of South California) for DN-IKKα(K44M) and DN-IKKβ(K49A); J. Jun Ninomiya-Tsuji (Lerner Research Institute) for DN-TAK1(K63W); Z. Cao (Tularik) for DN-IRAK1 (1–208); and the Mount Sinai School of Medicine Microscopy Shared Resource Facility. Supported by the US National Institutes of Health (R01 AI-05753 and R01 AI-074378 to A. Cerutti and S10RR09145), Catalan Institute for Research and Advanced Studies (A. Cerutti), Fundacio’ Institut Municipal d’Investigació Mèdica (A. Cerutti), Ministerio de Ciencia e Innovación (SAF 2008-02725 to A. Cerutti), The Irma T. Hirschl Charitable Trust (A. Cerutti), Comissionat per a Universitats i Recerca del Departament d’Innovació, Universitats i Empresa de la Generalitat de Catalunya (R.S.), Programa Juán de la Cierva (I.P.), Fondazione C. Golgi and Centro Immunodeficienze Mario di Martino (A. Plebani), TÁMOP (4.2.2-08/1-2008-0015 to L.M.), the US National Institutes of Health–National Cancer Institute (5R24 CA095823) and the National Science Foundation (DBI-9724504).

PY - 2010/9

Y1 - 2010/9

N2 - BAFF and APRIL are innate immune mediators that trigger immunoglobulin G (IgG) and IgA class-switch recombination (CSR) in B cells by engaging the receptor TACI. The mechanism that underlies CSR signaling by TACI remains unknown. Here we found that the cytoplasmic domain of TACI encompasses a conserved motif that bound MyD88, an adaptor that activates transcription factor NF-κB signaling pathways via a Toll-interleukin 1 (IL-1) receptor (TIR) domain. TACI lacks a TIR domain, yet triggered CSR via the DNA-editing enzyme AID by activating NF-κB through a Toll-like receptor (TLR)-like MyD88-IRAK1-IRAK4-TRAF6-TAK1 pathway. TACI-induced CSR was impaired in mice and humans lacking MyD88 or the kinase IRAK4, which indicates that MyD88 controls a B cell-intrinsic, TIR-independent, TACI-dependent pathway for immunoglobulin diversification.

AB - BAFF and APRIL are innate immune mediators that trigger immunoglobulin G (IgG) and IgA class-switch recombination (CSR) in B cells by engaging the receptor TACI. The mechanism that underlies CSR signaling by TACI remains unknown. Here we found that the cytoplasmic domain of TACI encompasses a conserved motif that bound MyD88, an adaptor that activates transcription factor NF-κB signaling pathways via a Toll-interleukin 1 (IL-1) receptor (TIR) domain. TACI lacks a TIR domain, yet triggered CSR via the DNA-editing enzyme AID by activating NF-κB through a Toll-like receptor (TLR)-like MyD88-IRAK1-IRAK4-TRAF6-TAK1 pathway. TACI-induced CSR was impaired in mice and humans lacking MyD88 or the kinase IRAK4, which indicates that MyD88 controls a B cell-intrinsic, TIR-independent, TACI-dependent pathway for immunoglobulin diversification.

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The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88

Résumé

Note bibliographique

ASJC Scopus Subject Areas

Accès au document

Autres fichiers et liens

Empreinte numérique

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