Memory T-cells and characterization of peripheral T-cell clones in acute Kawasaki disease

Kawasaki disease (KD) is a pediatric self-limited vasculitis characterized by immune-mediated destruction of the arterial wall and myocardium. Neither the trigger that incites the inflammation nor the switch that turns it off is known. To further our understanding of KD pathogenesis and the role of...

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Published inAutoimmunity (Chur, Switzerland) Vol. 43; no. 4; pp. 317 - 324
Main Authors Franco, Alessandra, Shimizu, Chisato, Tremoulet, Adriana H., Burns, Jane C.
Format Journal Article
LanguageEnglish
Published England Informa 01.06.2010
Taylor & Francis
Subjects
Online AccessGet full text
ISSN0891-6934
1607-842X
1607-842X
DOI10.3109/08916930903405891

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Abstract Kawasaki disease (KD) is a pediatric self-limited vasculitis characterized by immune-mediated destruction of the arterial wall and myocardium. Neither the trigger that incites the inflammation nor the switch that turns it off is known. To further our understanding of KD pathogenesis and the role of regulatory T-cells in modulating the inflammatory response, we studied circulating effector memory T-cells (CCR7 − and IL-15+ Tem) and central memory T-cells (CCR7+ and IL-15+ Tcm) in six KD subjects. In two of the subjects, we cloned the remaining T-cell population by limiting dilution. TaqMan analysis of Tem studied in two KD subjects suggested that Tem are pro-inflammatory CD4+T-helper 1 cells and CD8+ cytotoxic T-cells. Following memory T-cells over time, we defined that circulating Tem and Tcm are detectable during the acute phase in some KD subjects before treatment with intravenous immunoglobulin. Both Tem and Tcm expand rapidly within 2 weeks of treatment. The circulating Tem pool contracts, while Tcm further proliferate in the convalescent phase. Following depletion of memory T-cells, numerous T-cell clones were derived from two acute KD subjects. The large majority of these T-cells displayed the functional phenotype of peripherally induced regulatory T-cells (Treg). These findings provide insight into the nature and kinetics of the adaptive immune response in KD.
AbstractList Kawasaki disease (KD) is a pediatric self-limited vasculitis characterized by immune-mediated destruction of the arterial wall and myocardium. Neither the trigger that incites the inflammation nor the switch that turns it off is known. To further our understanding of KD pathogenesis and the role of regulatory T-cells in modulating the inflammatory response, we studied circulating effector memory T-cells (CCR7- and IL-15+ T(em)) and central memory T-cells (CCR7+ and IL-15+ T(cm)) in six KD subjects. In two of the subjects, we cloned the remaining T-cell population by limiting dilution. TaqMan analysis of T(em) studied in two KD subjects suggested that T(em) are pro-inflammatory CD4+T-helper 1 cells and CD8+ cytotoxic T-cells. Following memory T-cells over time, we defined that circulating T(em) and T(cm) are detectable during the acute phase in some KD subjects before treatment with intravenous immunoglobulin. Both T(em) and T(cm) expand rapidly within 2 weeks of treatment. The circulating T(em) pool contracts, while T(cm) further proliferate in the convalescent phase. Following depletion of memory T-cells, numerous T-cell clones were derived from two acute KD subjects. The large majority of these T-cells displayed the functional phenotype of peripherally induced regulatory T-cells (T(reg)). These findings provide insight into the nature and kinetics of the adaptive immune response in KD.Kawasaki disease (KD) is a pediatric self-limited vasculitis characterized by immune-mediated destruction of the arterial wall and myocardium. Neither the trigger that incites the inflammation nor the switch that turns it off is known. To further our understanding of KD pathogenesis and the role of regulatory T-cells in modulating the inflammatory response, we studied circulating effector memory T-cells (CCR7- and IL-15+ T(em)) and central memory T-cells (CCR7+ and IL-15+ T(cm)) in six KD subjects. In two of the subjects, we cloned the remaining T-cell population by limiting dilution. TaqMan analysis of T(em) studied in two KD subjects suggested that T(em) are pro-inflammatory CD4+T-helper 1 cells and CD8+ cytotoxic T-cells. Following memory T-cells over time, we defined that circulating T(em) and T(cm) are detectable during the acute phase in some KD subjects before treatment with intravenous immunoglobulin. Both T(em) and T(cm) expand rapidly within 2 weeks of treatment. The circulating T(em) pool contracts, while T(cm) further proliferate in the convalescent phase. Following depletion of memory T-cells, numerous T-cell clones were derived from two acute KD subjects. The large majority of these T-cells displayed the functional phenotype of peripherally induced regulatory T-cells (T(reg)). These findings provide insight into the nature and kinetics of the adaptive immune response in KD.
Kawasaki disease (KD) is a pediatric self-limited vasculitis characterized by immune-mediated destruction of the arterial wall and myocardium. Neither the trigger that incites the inflammation nor the switch that turns it off is known. To further our understanding of KD pathogenesis and the role of regulatory T-cells in modulating the inflammatory response, we studied circulating effector memory T-cells (CCR7 - and IL-15+ T super(em)) and central memory T-cells (CCR7+ and IL-15+ T super(cm)) in six KD subjects. In two of the subjects, we cloned the remaining T-cell population by limiting dilution. TaqMan analysis of T super(em) studied in two KD subjects suggested that T super(em) are pro-inflammatory CD4+T-helper 1 cells and CD8+ cytotoxic T-cells. Following memory T-cells over time, we defined that circulating T super(em) and T super(cm) are detectable during the acute phase in some KD subjects before treatment with intravenous immunoglobulin. Both T super(em) and T super(cm) expand rapidly within 2 weeks of treatment. The circulating T super(em) pool contracts, while T super(cm) further proliferate in the convalescent phase. Following depletion of memory T-cells, numerous T-cell clones were derived from two acute KD subjects. The large majority of these T-cells displayed the functional phenotype of peripherally induced regulatory T-cells (T super(reg)). These findings provide insight into the nature and kinetics of the adaptive immune response in KD.
Kawasaki disease (KD) is a pediatric self-limited vasculitis characterized by immune-mediated destruction of the arterial wall and myocardium. Neither the trigger that incites the inflammation nor the switch that turns it off is known. To further our understanding of KD pathogenesis and the role of regulatory T-cells in modulating the inflammatory response, we studied circulating effector memory T-cells (CCR7− and IL-15+ T em ) and central memory T-cells (CCR7+ and IL-15+ T cm ) in six KD subjects. In two of the subjects, we cloned the remaining T-cell population by limiting dilution. TaqMan analysis of T em studied in two KD subjects suggested that T em are pro-inflammatory CD4+ T-helper 1 cells and CD8+ cytotoxic T-cells. Following memory T-cells over time, we defined that circulating T em and T cm are detectable during the acute phase in some KD subjects before treatment with intravenous immunoglobulin. Both T em and T cm expand rapidly within 2 weeks of treatment. The circulating T em pool contracts, while T cm further proliferate in the convalescent phase. Following depletion of memory T-cells, numerous T-cell clones were derived from two acute KD subjects. The large majority of these T-cells displayed the functional phenotype of peripherally induced regulatory T-cells (T reg ). These findings provide insight into the nature and kinetics of the adaptive immune response in KD.
Kawasaki disease (KD) is a pediatric self-limited vasculitis characterized by immune-mediated destruction of the arterial wall and myocardium. Neither the trigger that incites the inflammation nor the switch that turns it off is known. To further our understanding of KD pathogenesis and the role of regulatory T-cells in modulating the inflammatory response, we studied circulating effector memory T-cells (CCR7 − and IL-15+ Tem) and central memory T-cells (CCR7+ and IL-15+ Tcm) in six KD subjects. In two of the subjects, we cloned the remaining T-cell population by limiting dilution. TaqMan analysis of Tem studied in two KD subjects suggested that Tem are pro-inflammatory CD4+T-helper 1 cells and CD8+ cytotoxic T-cells. Following memory T-cells over time, we defined that circulating Tem and Tcm are detectable during the acute phase in some KD subjects before treatment with intravenous immunoglobulin. Both Tem and Tcm expand rapidly within 2 weeks of treatment. The circulating Tem pool contracts, while Tcm further proliferate in the convalescent phase. Following depletion of memory T-cells, numerous T-cell clones were derived from two acute KD subjects. The large majority of these T-cells displayed the functional phenotype of peripherally induced regulatory T-cells (Treg). These findings provide insight into the nature and kinetics of the adaptive immune response in KD.
Kawasaki disease (KD) is a pediatric self-limited vasculitis characterized by immune-mediated destruction of the arterial wall and myocardium. Neither the trigger that incites the inflammation nor the switch that turns it off is known. To further our understanding of KD pathogenesis and the role of regulatory T-cells in modulating the inflammatory response, we studied circulating effector memory T-cells (CCR7- and IL-15+ T(em)) and central memory T-cells (CCR7+ and IL-15+ T(cm)) in six KD subjects. In two of the subjects, we cloned the remaining T-cell population by limiting dilution. TaqMan analysis of T(em) studied in two KD subjects suggested that T(em) are pro-inflammatory CD4+T-helper 1 cells and CD8+ cytotoxic T-cells. Following memory T-cells over time, we defined that circulating T(em) and T(cm) are detectable during the acute phase in some KD subjects before treatment with intravenous immunoglobulin. Both T(em) and T(cm) expand rapidly within 2 weeks of treatment. The circulating T(em) pool contracts, while T(cm) further proliferate in the convalescent phase. Following depletion of memory T-cells, numerous T-cell clones were derived from two acute KD subjects. The large majority of these T-cells displayed the functional phenotype of peripherally induced regulatory T-cells (T(reg)). These findings provide insight into the nature and kinetics of the adaptive immune response in KD.
Kawasaki disease (KD) is a pediatric self-limited vasculitis characterized by immune-mediated destruction of the arterial wall and myocardium. Neither the trigger that incites the inflammation nor the switch that turns it off is known. To further our understanding of KD pathogenesis and the role of regulatory T-cells in modulating the inflammatory response, we studied circulating effector memory T-cells (CCR7 − and IL-15+ T em ) and central memory T-cells (CCR7+ and IL-15+ T cm ) in six KD subjects. In two of the subjects, we cloned the remaining T-cell population by limiting dilution. TaqMan analysis of T em studied in two KD subjects suggested that T em are pro-inflammatory CD4+T-helper 1 cells and CD8+ cytotoxic T-cells. Following memory T-cells over time, we defined that circulating T em and T cm are detectable during the acute phase in some KD subjects before treatment with intravenous immunoglobulin. Both T em and T cm expand rapidly within 2 weeks of treatment. The circulating T em pool contracts, while T cm further proliferate in the convalescent phase. Following depletion of memory T-cells, numerous T-cell clones were derived from two acute KD subjects. The large majority of these T-cells displayed the functional phenotype of peripherally induced regulatory T-cells (T reg ). These findings provide insight into the nature and kinetics of the adaptive immune response in KD.
Author Tremoulet, Adriana H.
Burns, Jane C.
Franco, Alessandra
Shimizu, Chisato
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Snippet Kawasaki disease (KD) is a pediatric self-limited vasculitis characterized by immune-mediated destruction of the arterial wall and myocardium. Neither the...
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SubjectTerms Acute Disease
Adaptive Immunity
Clone Cells - cytology
Clone Cells - immunology
Female
Flow Cytometry
human T-cell clones
Humans
immune regulation
Immunologic Memory
Infant
Kawasaki disease
Male
Mucocutaneous Lymph Node Syndrome - immunology
T-cell memory
T-Lymphocytes - immunology
T-Lymphocytes, Regulatory - immunology
Tregs
Title Memory T-cells and characterization of peripheral T-cell clones in acute Kawasaki disease
URI https://www.tandfonline.com/doi/abs/10.3109/08916930903405891
https://www.ncbi.nlm.nih.gov/pubmed/20166878
https://www.proquest.com/docview/1356934357
https://www.proquest.com/docview/733135898
https://pubmed.ncbi.nlm.nih.gov/PMC2871072
Volume 43
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