Interleukin-7 Is a Survival Factor for CD4+ CD25+ T-Cells and Is Expressed by Diabetes-Suppressive Dendritic Cells
Interleukin-7 Is a Survival Factor for CD4 + CD25 + T-Cells and Is Expressed by Diabetes-Suppressive Dendritic Cells Jo Harnaha 1 , Jennifer Machen 1 , Marietta Wright 1 , Robert Lakomy 1 , Alexis Styche 1 , Massimo Trucco 1 , Sami Makaroun 1 and Nick Giannoukakis 1 2 1 Department of Pediatrics, Div...
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Published in | Diabetes (New York, N.Y.) Vol. 55; no. 1; pp. 158 - 170 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Diabetes Association
01.01.2006
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Abstract | Interleukin-7 Is a Survival Factor for CD4 + CD25 + T-Cells and Is Expressed by Diabetes-Suppressive Dendritic Cells
Jo Harnaha 1 ,
Jennifer Machen 1 ,
Marietta Wright 1 ,
Robert Lakomy 1 ,
Alexis Styche 1 ,
Massimo Trucco 1 ,
Sami Makaroun 1 and
Nick Giannoukakis 1 2
1 Department of Pediatrics, Division of Immunogenetics, Diabetes Institute, University of Pittsburgh School of Medicine, Pittsburgh,
Pennsylvania
2 Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania
Address correspondence and reprint requests to Nick Giannoukakis, PhD, Department of Pathology, University of Pittsburgh School
of Medicine, Diabetes Institute, Rangos Research Center, 3460 Fifth Ave., Pittsburgh, PA 15213. E-mail: ngiann1{at}pitt.edu
Abstract
Dendritic cells can facilitate allograft survival and prevent autoimmunity via direct and indirect cell-mediated mechanisms.
Recent studies demonstrate that immunoregulatory dendritic cells (iDCs) confer immune hyporesponsiveness in part through CD4 + CD25 + T regulatory cells (Tregs). Herein, we provide evidence to support the hypothesis that dendritic cells derived from NOD mice
and engineered ex vivo to exhibit suppressed expression of the CD40, CD80, and CD86 costimulatory molecules motivate an increase
in the prevalence of regulatory CD4 + CD25 + T-cells via interleukin (IL)-7. Unlike control dendritic cells, these dendritic cells expressed significant levels of IL-7.
Exogenous addition of IL-7 to NOD T-cells did not promote expansion or proliferation, but instead selectively maintained the
number of CD4 + CD25 + T-cells by inhibiting activation of apoptosis in these cells. In vitro, IL-7 receptor α-chain (IL-7Rα) was expressed at significantly
higher levels on CD4 + CD25 + T-cells compared with CD4 + CD25 − T-cells irrespective of resting or stimulated state. In vivo, CD4 + CD25 + T-cells obtained from NOD-scid mice reconstituted with ex vivo engineered iDCs and NOD splenocytes expressed significantly
higher levels of IL-7Rα compared with levels in the CD4 + CD25 − subset, especially in diabetes-suppressive dendritic cell–administered NOD-scid recipients. Taken together, our data suggest
a novel mechanism by which iDCs delay autoimmunity through the CD4 + CD25 + Treg pathway and suggest IL-7 as a survival factor for these putative Tregs, which express the α-chain of its receptor at
considerably higher levels than CD4 + CD25 − T-cells.
CFSE, carboxyfluorescein ester
FACS, fluorescence-activated cell sorter
iDC, immunoregulatory dendritic cell
IL, interleukin
STAT, signal transducer and activation of transcription
Treg, T regulatory cell
Footnotes
Accepted September 23, 2005.
Received March 16, 2005.
DIABETES |
---|---|
AbstractList | Dendritic cells can facilitate allograft survival and prevent autoimmunity via direct and indirect cell-mediated mechanisms. Recent studies demonstrate that immunoregulatory dendritic cells (iDCs) confer immune hyporesponsiveness in part through CD4+ CD25+ T regulatory cells (Tregs). Herein, we provide evidence to support the hypothesis that dendritic cells derived from NOD mice and engineered ex vivo to exhibit suppressed expression of the CD40, CD80, and CD86 costimulatory molecules motivate an increase in the prevalence of regulatory CD4+ CD25+ T-cells via interleukin (IL)-7. Unlike control dendritic cells, these dendritic cells expressed significant levels of IL-7. Exogenous addition of IL-7 to NOD T-cells did not promote expansion or proliferation, but instead selectively maintained the number of CD4+ CD25+ T-cells by inhibiting activation of apoptosis in these cells. In vitro, IL-7 receptor α-chain (IL-7Rα) was expressed at significantly higher levels on CD4+ CD25+ T-cells compared with CD4+ CD25− T-cells irrespective of resting or stimulated state. In vivo, CD4+ CD25+ T-cells obtained from NOD-scid mice reconstituted with ex vivo engineered iDCs and NOD splenocytes expressed significantly higher levels of IL-7Rα compared with levels in the CD4+ CD25− subset, especially in diabetes-suppressive dendritic cell–administered NOD-scid recipients. Taken together, our data suggest a novel mechanism by which iDCs delay autoimmunity through the CD4+ CD25+ Treg pathway and suggest IL-7 as a survival factor for these putative Tregs, which express the α-chain of its receptor at considerably higher levels than CD4+ CD25− T-cells. Dendritic cells can facilitate allograft survival and prevent autoimmunity via direct and indirect cell-mediated mechanisms. Recent studies demonstrate that immunoregulatory dendritic cells (iDCs) confer immune hyporesponsiveness in part through CD4(+) CD25(+) T regulatory cells (Tregs). Herein, we provide evidence to support the hypothesis that dendritic cells derived from NOD mice and engineered ex vivo to exhibit suppressed expression of the CD40, CD80, and CD86 costimulatory molecules motivate an increase in the prevalence of regulatory CD4(+) CD25(+) T-cells via interleukin (IL)-7. Unlike control dendritic cells, these dendritic cells expressed significant levels of IL-7. Exogenous addition of IL-7 to NOD T-cells did not promote expansion or proliferation, but instead selectively maintained the number of CD4(+) CD25(+) T-cells by inhibiting activation of apoptosis in these cells. In vitro, IL-7 receptor alpha-chain (IL-7Ralpha) was expressed at significantly higher levels on CD4(+) CD25(+) T-cells compared with CD4(+) CD25(-) T-cells irrespective of resting or stimulated state. In vivo, CD4(+) CD25(+) T-cells obtained from NOD-scid mice reconstituted with ex vivo engineered iDCs and NOD splenocytes expressed significantly higher levels of IL-7Ralpha compared with levels in the CD4(+) CD25(-) subset, especially in diabetes-suppressive dendritic cell-administered NOD-scid recipients. Taken together, our data suggest a novel mechanism by which iDCs delay autoimmunity through the CD4(+) CD25(+) Treg pathway and suggest IL-7 as a survival factor for these putative Tregs, which express the alpha-chain of its receptor at considerably higher levels than CD4(+) CD25(-) T-cells. Interleukin-7 Is a Survival Factor for CD4 + CD25 + T-Cells and Is Expressed by Diabetes-Suppressive Dendritic Cells Jo Harnaha 1 , Jennifer Machen 1 , Marietta Wright 1 , Robert Lakomy 1 , Alexis Styche 1 , Massimo Trucco 1 , Sami Makaroun 1 and Nick Giannoukakis 1 2 1 Department of Pediatrics, Division of Immunogenetics, Diabetes Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 2 Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania Address correspondence and reprint requests to Nick Giannoukakis, PhD, Department of Pathology, University of Pittsburgh School of Medicine, Diabetes Institute, Rangos Research Center, 3460 Fifth Ave., Pittsburgh, PA 15213. E-mail: ngiann1{at}pitt.edu Abstract Dendritic cells can facilitate allograft survival and prevent autoimmunity via direct and indirect cell-mediated mechanisms. Recent studies demonstrate that immunoregulatory dendritic cells (iDCs) confer immune hyporesponsiveness in part through CD4 + CD25 + T regulatory cells (Tregs). Herein, we provide evidence to support the hypothesis that dendritic cells derived from NOD mice and engineered ex vivo to exhibit suppressed expression of the CD40, CD80, and CD86 costimulatory molecules motivate an increase in the prevalence of regulatory CD4 + CD25 + T-cells via interleukin (IL)-7. Unlike control dendritic cells, these dendritic cells expressed significant levels of IL-7. Exogenous addition of IL-7 to NOD T-cells did not promote expansion or proliferation, but instead selectively maintained the number of CD4 + CD25 + T-cells by inhibiting activation of apoptosis in these cells. In vitro, IL-7 receptor α-chain (IL-7Rα) was expressed at significantly higher levels on CD4 + CD25 + T-cells compared with CD4 + CD25 − T-cells irrespective of resting or stimulated state. In vivo, CD4 + CD25 + T-cells obtained from NOD-scid mice reconstituted with ex vivo engineered iDCs and NOD splenocytes expressed significantly higher levels of IL-7Rα compared with levels in the CD4 + CD25 − subset, especially in diabetes-suppressive dendritic cell–administered NOD-scid recipients. Taken together, our data suggest a novel mechanism by which iDCs delay autoimmunity through the CD4 + CD25 + Treg pathway and suggest IL-7 as a survival factor for these putative Tregs, which express the α-chain of its receptor at considerably higher levels than CD4 + CD25 − T-cells. CFSE, carboxyfluorescein ester FACS, fluorescence-activated cell sorter iDC, immunoregulatory dendritic cell IL, interleukin STAT, signal transducer and activation of transcription Treg, T regulatory cell Footnotes Accepted September 23, 2005. Received March 16, 2005. DIABETES |
Author | Robert Lakomy Massimo Trucco Sami Makaroun Marietta Wright Jo Harnaha Nick Giannoukakis Jennifer Machen Alexis Styche |
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Snippet | Interleukin-7 Is a Survival Factor for CD4 + CD25 + T-Cells and Is Expressed by Diabetes-Suppressive Dendritic Cells
Jo Harnaha 1 ,
Jennifer Machen 1 ,... Dendritic cells can facilitate allograft survival and prevent autoimmunity via direct and indirect cell-mediated mechanisms. Recent studies demonstrate that... |
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SubjectTerms | Animals Apoptosis Biological and medical sciences CD4-Positive T-Lymphocytes - cytology CD4-Positive T-Lymphocytes - drug effects CD4-Positive T-Lymphocytes - metabolism Cell Survival - drug effects Dendritic Cells - metabolism Diabetes Mellitus, Type 1 - metabolism Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Gene Expression Regulation Humans Interleukin-7 - genetics Interleukin-7 - metabolism Interleukin-7 - pharmacology Medical sciences Mice Mice, Inbred NOD Receptors, Interleukin-2 - metabolism Receptors, Interleukin-7 - metabolism |
Title | Interleukin-7 Is a Survival Factor for CD4+ CD25+ T-Cells and Is Expressed by Diabetes-Suppressive Dendritic Cells |
URI | http://diabetes.diabetesjournals.org/content/55/1/158.abstract https://www.ncbi.nlm.nih.gov/pubmed/16380489 https://search.proquest.com/docview/67599097 |
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