CD8 T cells induce T-bet-dependent migration toward CXCR3 ligands by differentiated B cells produced during responses to alum-protein vaccines

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CD8 T cells induce T-bet-dependent migration toward CXCR3 ligands by differentiated B cells produced during responses to alum-protein vaccines. / Serre, Karine; Cunningham, Adam F; Coughlan, Ruth E; Lino, Andreia C; Rot, Antal; Hub, Elin; Moser, Katrin; Manz, Rudolf; Ferraro, Alastair; Bird, Roger; Toellner, Kai-Michael; Demengeot, Jocelyne; MacLennan, Ian C M; Mohr, Elodie.

In: Blood, Vol. 120, No. 23, 29.11.2012, p. 4552-9.

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@article{f2f0fda6b42f4503b09b6317f78f3d49,
title = "CD8 T cells induce T-bet-dependent migration toward CXCR3 ligands by differentiated B cells produced during responses to alum-protein vaccines",
abstract = "Antibody-forming cells (AFCs) expressing the chemokine receptor CXCR3 are recruited to sites of inflammation where they help clear pathogens but may participate in autoimmune diseases. Here we identify a mechanism that induces CXCR3 expression by AFC and germinal center (GC) B cells. This happens when CD8 T cells are recruited into CD4 T cell-dependent B-cell responses. Ovalbumin-specific CD4 T cells (OTII) were transferred alone or with ovalbumin-specific CD8 T cells (OTI) and the response to subcutaneous alum-precipitated ovalbumin was followed in the draining lymph nodes. OTII cells alone induce T helper 2-associated class switching to IgG1, but few AFC or GC B cells express CXCR3. By contrast, OTI-derived IFN-γ induces most responding GC B cells and AFCs to express high levels of CXCR3, and diverse switching to IgG2a, IgG2b, with some IgG1. Up-regulation of CXCR3 by GC B cells and AFCs and their migration toward its ligand CXCL10 are shown to depend on B cells' intrinsic T-bet, a transcription factor downstream of the IFN-γR signaling. This model clarifies how precursors of long-lived AFCs and memory B cells acquire CXCR3 that causes their migration to inflammatory foci.",
keywords = "Cell Movement, Ovalbumin, Animals, Interferon-gamma, Cell Differentiation, Mice, Th2 Cells, Reverse Transcriptase Polymerase Chain Reaction, B-Lymphocytes, T-Box Domain Proteins, CD4-Positive T-Lymphocytes, Immunization, Alum Compounds, Receptors, CXCR3, Adoptive Transfer, CD8-Positive T-Lymphocytes, Germinal Center, Mice, Inbred C57BL, Flow Cytometry, Vaccines, Up-Regulation, Chemokine CXCL10, Ligands",
author = "Karine Serre and Cunningham, {Adam F} and Coughlan, {Ruth E} and Lino, {Andreia C} and Antal Rot and Elin Hub and Katrin Moser and Rudolf Manz and Alastair Ferraro and Roger Bird and Kai-Michael Toellner and Jocelyne Demengeot and MacLennan, {Ian C M} and Elodie Mohr",
year = "2012",
month = nov,
day = "29",
doi = "10.1182/blood-2012-03-417733",
language = "English",
volume = "120",
pages = "4552--9",
journal = "Blood",
issn = "0006-4971",
publisher = "American Society of Hematology",
number = "23",

}

RIS

TY - JOUR

T1 - CD8 T cells induce T-bet-dependent migration toward CXCR3 ligands by differentiated B cells produced during responses to alum-protein vaccines

AU - Serre, Karine

AU - Cunningham, Adam F

AU - Coughlan, Ruth E

AU - Lino, Andreia C

AU - Rot, Antal

AU - Hub, Elin

AU - Moser, Katrin

AU - Manz, Rudolf

AU - Ferraro, Alastair

AU - Bird, Roger

AU - Toellner, Kai-Michael

AU - Demengeot, Jocelyne

AU - MacLennan, Ian C M

AU - Mohr, Elodie

PY - 2012/11/29

Y1 - 2012/11/29

N2 - Antibody-forming cells (AFCs) expressing the chemokine receptor CXCR3 are recruited to sites of inflammation where they help clear pathogens but may participate in autoimmune diseases. Here we identify a mechanism that induces CXCR3 expression by AFC and germinal center (GC) B cells. This happens when CD8 T cells are recruited into CD4 T cell-dependent B-cell responses. Ovalbumin-specific CD4 T cells (OTII) were transferred alone or with ovalbumin-specific CD8 T cells (OTI) and the response to subcutaneous alum-precipitated ovalbumin was followed in the draining lymph nodes. OTII cells alone induce T helper 2-associated class switching to IgG1, but few AFC or GC B cells express CXCR3. By contrast, OTI-derived IFN-γ induces most responding GC B cells and AFCs to express high levels of CXCR3, and diverse switching to IgG2a, IgG2b, with some IgG1. Up-regulation of CXCR3 by GC B cells and AFCs and their migration toward its ligand CXCL10 are shown to depend on B cells' intrinsic T-bet, a transcription factor downstream of the IFN-γR signaling. This model clarifies how precursors of long-lived AFCs and memory B cells acquire CXCR3 that causes their migration to inflammatory foci.

AB - Antibody-forming cells (AFCs) expressing the chemokine receptor CXCR3 are recruited to sites of inflammation where they help clear pathogens but may participate in autoimmune diseases. Here we identify a mechanism that induces CXCR3 expression by AFC and germinal center (GC) B cells. This happens when CD8 T cells are recruited into CD4 T cell-dependent B-cell responses. Ovalbumin-specific CD4 T cells (OTII) were transferred alone or with ovalbumin-specific CD8 T cells (OTI) and the response to subcutaneous alum-precipitated ovalbumin was followed in the draining lymph nodes. OTII cells alone induce T helper 2-associated class switching to IgG1, but few AFC or GC B cells express CXCR3. By contrast, OTI-derived IFN-γ induces most responding GC B cells and AFCs to express high levels of CXCR3, and diverse switching to IgG2a, IgG2b, with some IgG1. Up-regulation of CXCR3 by GC B cells and AFCs and their migration toward its ligand CXCL10 are shown to depend on B cells' intrinsic T-bet, a transcription factor downstream of the IFN-γR signaling. This model clarifies how precursors of long-lived AFCs and memory B cells acquire CXCR3 that causes their migration to inflammatory foci.

KW - Cell Movement

KW - Ovalbumin

KW - Animals

KW - Interferon-gamma

KW - Cell Differentiation

KW - Mice

KW - Th2 Cells

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - B-Lymphocytes

KW - T-Box Domain Proteins

KW - CD4-Positive T-Lymphocytes

KW - Immunization

KW - Alum Compounds

KW - Receptors, CXCR3

KW - Adoptive Transfer

KW - CD8-Positive T-Lymphocytes

KW - Germinal Center

KW - Mice, Inbred C57BL

KW - Flow Cytometry

KW - Vaccines

KW - Up-Regulation

KW - Chemokine CXCL10

KW - Ligands

U2 - 10.1182/blood-2012-03-417733

DO - 10.1182/blood-2012-03-417733

M3 - Article

C2 - 23065152

VL - 120

SP - 4552

EP - 4559

JO - Blood

JF - Blood

SN - 0006-4971

IS - 23

ER -