Blood CD4+CD45RO+CXCR5+ T cells are decreased but partially functional in signal transducer and activator of transcription 3 deficiency
The generation of high-affinity antibodies requires the presence of a population of CD4+ T cells (follicular TH [TFH] cells) in the lymph node follicles. These cells differ from TH1, TH2, and TH17 effector cells in that they strongly express activation markers and the chemokine receptor CXCR5 and se...
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| Published in | Journal of allergy and clinical immunology Vol. 131; no. 4; pp. 1146 - 1156.e5 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York, NY
Mosby, Inc
01.04.2013
Elsevier Elsevier Limited |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0091-6749 1097-6825 1097-6825 |
| DOI | 10.1016/j.jaci.2012.12.1519 |
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| Abstract | The generation of high-affinity antibodies requires the presence of a population of CD4+ T cells (follicular TH [TFH] cells) in the lymph node follicles. These cells differ from TH1, TH2, and TH17 effector cells in that they strongly express activation markers and the chemokine receptor CXCR5 and secrete large amounts of IL-21 and CXCL13. Small numbers of nonactivated CD4+CD45RO+CXCR5+ T cells are also found in the blood.
We sought to obtain in vitro a population close to the TFH cells and to study the presence of this cell population among patients with autosomal dominant hyper-IgE syndrome carrying heterozygous signal transducer and activator of transcription 3 (STAT3) mutations that impair the IL-21 signaling required for B-cell differentiation.
CD4+CD45RO+CXCR5+ T cells were isolated from blood and activated by CD3/T-cell receptor.
We found that CD4+CD45RO+CXCR5+ activated T cells corresponding to circulating bona fide memory TFH cells and that STAT3-deficient patients have abnormally low numbers of “TFH-like” blood T cells. However, STAT3-deficient TFH cells have much the same phenotypic and functional characteristics as TFH cells from healthy control subjects. The ability of STAT3-deficient TFH cells to produce IL-21 on CD28/T-cell receptor activation and to proliferate did not differ from that observed for control TFH cells in vitro. Although the STAT3-deficient TFH cells were also able to help control B cells to produce IgG and IgA, induction of IgG production by naive B cells was impaired.
Heterozygous mutations in STAT3 lead to reduced numbers of circulating TFH-like cells, a finding that might account (at least in part) for the observed defect in antibody production. |
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| AbstractList | The generation of high-affinity antibodies requires the presence of a population of CD4+ T cells (follicular TH [TFH] cells) in the lymph node follicles. These cells differ from TH1, TH2, and TH17 effector cells in that they strongly express activation markers and the chemokine receptor CXCR5 and secrete large amounts of IL-21 and CXCL13. Small numbers of nonactivated CD4+CD45RO+CXCR5+ T cells are also found in the blood.
We sought to obtain in vitro a population close to the TFH cells and to study the presence of this cell population among patients with autosomal dominant hyper-IgE syndrome carrying heterozygous signal transducer and activator of transcription 3 (STAT3) mutations that impair the IL-21 signaling required for B-cell differentiation.
CD4+CD45RO+CXCR5+ T cells were isolated from blood and activated by CD3/T-cell receptor.
We found that CD4+CD45RO+CXCR5+ activated T cells corresponding to circulating bona fide memory TFH cells and that STAT3-deficient patients have abnormally low numbers of “TFH-like” blood T cells. However, STAT3-deficient TFH cells have much the same phenotypic and functional characteristics as TFH cells from healthy control subjects. The ability of STAT3-deficient TFH cells to produce IL-21 on CD28/T-cell receptor activation and to proliferate did not differ from that observed for control TFH cells in vitro. Although the STAT3-deficient TFH cells were also able to help control B cells to produce IgG and IgA, induction of IgG production by naive B cells was impaired.
Heterozygous mutations in STAT3 lead to reduced numbers of circulating TFH-like cells, a finding that might account (at least in part) for the observed defect in antibody production. Background The generation of high-affinity antibodies requires the presence of a population of CD4+T cells (follicular TH[TFH] cells) in the lymph node follicles. These cells differ from TH1, TH2, and TH17 effector cells in that they strongly express activation markers and the chemokine receptor CXCR5 and secrete large amounts of IL-21 and CXCL13. Small numbers of nonactivated CD4+CD45RO+CXCR5+T cells are also found in the blood. Objective We sought to obtainin vitroa population close to the TFHcells and to study the presence of this cell population among patients with autosomal dominant hyper-IgE syndrome carrying heterozygous signal transducer and activator of transcription 3(STAT3)mutations that impair the IL-21 signaling required for B-cell differentiation. Methods CD4+CD45RO+CXCR5+T cells were isolated from blood and activated by CD3/T-cell receptor. Results We found that CD4+CD45RO+CXCR5+activated T cells corresponding to circulatingbona fidememory TFHcells and that STAT3-deficient patients have abnormally low numbers of "TFH-like" blood T cells. However, STAT3-deficient TFHcells have much the same phenotypic and functional characteristics as TFHcells from healthy control subjects. The ability of STAT3-deficient TFHcells to produce IL-21 on CD28/T-cell receptor activation and to proliferate did not differ from that observed for control TFHcellsin vitro. Although the STAT3-deficient TFHcells were also able to help control B cells to produce IgG and IgA, induction of IgG production by naive B cells was impaired. Conclusion Heterozygous mutations inSTAT3lead to reduced numbers of circulating TFH-like cells, a finding that might account (at least in part) for the observed defect in antibody production. The generation of high-affinity antibodies requires the presence of a population of CD4+ T cells (follicular TH [TFH] cells) in the lymph node follicles. These cells differ from TH1, TH2, and TH17 effector cells in that they strongly express activation markers and the chemokine receptor CXCR5 and secrete large amounts of IL-21 and CXCL13. Small numbers of nonactivated CD4+CD45RO+CXCR5+ T cells are also found in the blood.BACKGROUNDThe generation of high-affinity antibodies requires the presence of a population of CD4+ T cells (follicular TH [TFH] cells) in the lymph node follicles. These cells differ from TH1, TH2, and TH17 effector cells in that they strongly express activation markers and the chemokine receptor CXCR5 and secrete large amounts of IL-21 and CXCL13. Small numbers of nonactivated CD4+CD45RO+CXCR5+ T cells are also found in the blood.We sought to obtain in vitro a population close to the TFH cells and to study the presence of this cell population among patients with autosomal dominant hyper-IgE syndrome carrying heterozygous signal transducer and activator of transcription 3 (STAT3) mutations that impair the IL-21 signaling required for B-cell differentiation.OBJECTIVEWe sought to obtain in vitro a population close to the TFH cells and to study the presence of this cell population among patients with autosomal dominant hyper-IgE syndrome carrying heterozygous signal transducer and activator of transcription 3 (STAT3) mutations that impair the IL-21 signaling required for B-cell differentiation.CD4+CD45RO+CXCR5+ T cells were isolated from blood and activated by CD3/T-cell receptor.METHODSCD4+CD45RO+CXCR5+ T cells were isolated from blood and activated by CD3/T-cell receptor.We found that CD4+CD45RO+CXCR5+ activated T cells corresponding to circulating bona fide memory TFH cells and that STAT3-deficient patients have abnormally low numbers of "TFH-like" blood T cells. However, STAT3-deficient TFH cells have much the same phenotypic and functional characteristics as TFH cells from healthy control subjects. The ability of STAT3-deficient TFH cells to produce IL-21 on CD28/T-cell receptor activation and to proliferate did not differ from that observed for control TFH cells in vitro. Although the STAT3-deficient TFH cells were also able to help control B cells to produce IgG and IgA, induction of IgG production by naive B cells was impaired.RESULTSWe found that CD4+CD45RO+CXCR5+ activated T cells corresponding to circulating bona fide memory TFH cells and that STAT3-deficient patients have abnormally low numbers of "TFH-like" blood T cells. However, STAT3-deficient TFH cells have much the same phenotypic and functional characteristics as TFH cells from healthy control subjects. The ability of STAT3-deficient TFH cells to produce IL-21 on CD28/T-cell receptor activation and to proliferate did not differ from that observed for control TFH cells in vitro. Although the STAT3-deficient TFH cells were also able to help control B cells to produce IgG and IgA, induction of IgG production by naive B cells was impaired.Heterozygous mutations in STAT3 lead to reduced numbers of circulating TFH-like cells, a finding that might account (at least in part) for the observed defect in antibody production.CONCLUSIONHeterozygous mutations in STAT3 lead to reduced numbers of circulating TFH-like cells, a finding that might account (at least in part) for the observed defect in antibody production. Background The generation of high-affinity antibodies requires the presence of a population of CD4+ T cells (follicular TH [TFH ] cells) in the lymph node follicles. These cells differ from TH 1, TH 2, and TH 17 effector cells in that they strongly express activation markers and the chemokine receptor CXCR5 and secrete large amounts of IL-21 and CXCL13. Small numbers of nonactivated CD4+ CD45RO+ CXCR5+ T cells are also found in the blood. Objective We sought to obtain in vitro a population close to the TFH cells and to study the presence of this cell population among patients with autosomal dominant hyper-IgE syndrome carrying heterozygous signal transducer and activator of transcription 3 (STAT3) mutations that impair the IL-21 signaling required for B-cell differentiation. Methods CD4+ CD45RO+ CXCR5+ T cells were isolated from blood and activated by CD3/T-cell receptor. Results We found that CD4+ CD45RO+ CXCR5+ activated T cells corresponding to circulating bona fide memory TFH cells and that STAT3-deficient patients have abnormally low numbers of “TFH -like” blood T cells. However, STAT3-deficient TFH cells have much the same phenotypic and functional characteristics as TFH cells from healthy control subjects. The ability of STAT3-deficient TFH cells to produce IL-21 on CD28/T-cell receptor activation and to proliferate did not differ from that observed for control TFH cells in vitro . Although the STAT3-deficient TFH cells were also able to help control B cells to produce IgG and IgA, induction of IgG production by naive B cells was impaired. Conclusion Heterozygous mutations in STAT3 lead to reduced numbers of circulating TFH -like cells, a finding that might account (at least in part) for the observed defect in antibody production. BACKGROUND: The generation of high-affinity antibodies requires the presence of a population of CD4⁺ T cells (follicular TH [TFH] cells) in the lymph node follicles. These cells differ from TH1, TH2, and TH17 effector cells in that they strongly express activation markers and the chemokine receptor CXCR5 and secrete large amounts of IL-21 and CXCL13. Small numbers of nonactivated CD4⁺CD45RO⁺CXCR5⁺ T cells are also found in the blood. OBJECTIVE: We sought to obtain in vitro a population close to the TFH cells and to study the presence of this cell population among patients with autosomal dominant hyper-IgE syndrome carrying heterozygous signal transducer and activator of transcription 3 (STAT3) mutations that impair the IL-21 signaling required for B-cell differentiation. METHODS: CD4⁺CD45RO⁺CXCR5⁺ T cells were isolated from blood and activated by CD3/T-cell receptor. RESULTS: We found that CD4⁺CD45RO⁺CXCR5⁺ activated T cells corresponding to circulating bona fide memory TFH cells and that STAT3-deficient patients have abnormally low numbers of “TFH-like” blood T cells. However, STAT3-deficient TFH cells have much the same phenotypic and functional characteristics as TFH cells from healthy control subjects. The ability of STAT3-deficient TFH cells to produce IL-21 on CD28/T-cell receptor activation and to proliferate did not differ from that observed for control TFH cells in vitro. Although the STAT3-deficient TFH cells were also able to help control B cells to produce IgG and IgA, induction of IgG production by naive B cells was impaired. CONCLUSION: Heterozygous mutations in STAT3 lead to reduced numbers of circulating TFH-like cells, a finding that might account (at least in part) for the observed defect in antibody production. The generation of high-affinity antibodies requires the presence of a population of CD4+ T cells (follicular TH [TFH] cells) in the lymph node follicles. These cells differ from TH1, TH2, and TH17 effector cells in that they strongly express activation markers and the chemokine receptor CXCR5 and secrete large amounts of IL-21 and CXCL13. Small numbers of nonactivated CD4+CD45RO+CXCR5+ T cells are also found in the blood. We sought to obtain in vitro a population close to the TFH cells and to study the presence of this cell population among patients with autosomal dominant hyper-IgE syndrome carrying heterozygous signal transducer and activator of transcription 3 (STAT3) mutations that impair the IL-21 signaling required for B-cell differentiation. CD4+CD45RO+CXCR5+ T cells were isolated from blood and activated by CD3/T-cell receptor. We found that CD4+CD45RO+CXCR5+ activated T cells corresponding to circulating bona fide memory TFH cells and that STAT3-deficient patients have abnormally low numbers of "TFH-like" blood T cells. However, STAT3-deficient TFH cells have much the same phenotypic and functional characteristics as TFH cells from healthy control subjects. The ability of STAT3-deficient TFH cells to produce IL-21 on CD28/T-cell receptor activation and to proliferate did not differ from that observed for control TFH cells in vitro. Although the STAT3-deficient TFH cells were also able to help control B cells to produce IgG and IgA, induction of IgG production by naive B cells was impaired. Heterozygous mutations in STAT3 lead to reduced numbers of circulating TFH-like cells, a finding that might account (at least in part) for the observed defect in antibody production. |
| Author | Picard, Capucine Kracker, Sven Durandy, Anne Fischer, Alain Mazerolles, Fabienne |
| Author_xml | – sequence: 1 givenname: Fabienne surname: Mazerolles fullname: Mazerolles, Fabienne email: fabienne.mazerolles@inserm.fr organization: INSERM U768, Paris, France – sequence: 2 givenname: Capucine surname: Picard fullname: Picard, Capucine organization: University Sorbonne Paris Cité, Paris Descartes, Institut Imagine, Necker Medicine Faculty, Paris, France – sequence: 3 givenname: Sven surname: Kracker fullname: Kracker, Sven organization: INSERM U768, Paris, France – sequence: 4 givenname: Alain surname: Fischer fullname: Fischer, Alain organization: INSERM U768, Paris, France – sequence: 5 givenname: Anne surname: Durandy fullname: Durandy, Anne organization: INSERM U768, Paris, France |
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| Keywords | Human CD40L CD62L signal transducer and activator of transcription 3 deficiency CSR cell activation STAT3 ICOSL T cells SEB Bcl6 TFH naive B cells GC ICOS IL-21R PD-1 Inducible costimulator ligand Programmed death 1 Germinal center Signal transducer and activator of transcription 3 L-selectin B-cell lymphoma 6 IL-21 receptor Inducible costimulator T FH Class-switch recombination CD40 ligand Follicular T H Staphylococcal enterotoxin B Immunopathology Deficiency Naive cell Activation B-Lymphocyte Blood cell Immunology Transcription factor STAT3 T-Lymphocyte |
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| Snippet | The generation of high-affinity antibodies requires the presence of a population of CD4+ T cells (follicular TH [TFH] cells) in the lymph node follicles. These... Background The generation of high-affinity antibodies requires the presence of a population of CD4+ T cells (follicular TH [TFH ] cells) in the lymph node... Background The generation of high-affinity antibodies requires the presence of a population of CD4+T cells (follicular TH[TFH] cells) in the lymph node... BACKGROUND: The generation of high-affinity antibodies requires the presence of a population of CD4⁺ T cells (follicular TH [TFH] cells) in the lymph node... |
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| SubjectTerms | Adolescent Adult Allergy and Immunology antibodies antibody formation Antigens B-lymphocytes B-Lymphocytes - immunology B-Lymphocytes - metabolism B-Lymphocytes - pathology Biological and medical sciences Blood CD4-positive T-lymphocytes cell activation Cell Differentiation chemokine CXCL13 Child CXCR5 receptor Cytokines Female functional properties Fundamental and applied biological sciences. Psychology Fundamental immunology Gene Expression heterozygosity Heterozygote Human Humans Immune system immunoglobulin A Immunoglobulin A - biosynthesis Immunoglobulin A - immunology immunoglobulin G Immunoglobulin G - biosynthesis Immunoglobulin G - immunology Immunoglobulins Immunopathology Interleukins - biosynthesis Interleukins - immunology Job Syndrome - genetics Job Syndrome - immunology Job Syndrome - metabolism Job Syndrome - pathology Leukocyte Common Antigens - genetics Leukocyte Common Antigens - immunology Ligands lymph nodes Lymphocyte Activation Lymphocyte Count Lymphocytes Male Medical sciences Middle Aged Mutation naive B cells patients Receptors, CXCR5 - genetics Receptors, CXCR5 - immunology Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis signal transducer and activator of transcription 3 deficiency Signal Transduction STAT3 Transcription Factor - deficiency STAT3 Transcription Factor - genetics STAT3 Transcription Factor - immunology T cells T-Lymphocyte Subsets - immunology T-Lymphocyte Subsets - metabolism T-Lymphocyte Subsets - pathology transcription (genetics) transcription factors |
| Title | Blood CD4+CD45RO+CXCR5+ T cells are decreased but partially functional in signal transducer and activator of transcription 3 deficiency |
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