Expansion of Human Regulatory T-Cells From Patients With Type 1 Diabetes
Expansion of Human Regulatory T-Cells From Patients With Type 1 Diabetes Amy L. Putnam 1 , Todd M. Brusko 1 , Michael R. Lee 1 , Weihong Liu 1 , Gregory L. Szot 1 , Taumoha Ghosh 1 , Mark A. Atkinson 2 and Jeffrey A. Bluestone 1 1 Diabetes Center at the University of California, San Francisco (UCSF)...
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| Vydáno v: | Diabetes (New York, N.Y.) Ročník 58; číslo 3; s. 652 - 662 |
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| Hlavní autoři: | , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
American Diabetes Association
01.03.2009
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| ISSN: | 0012-1797, 1939-327X, 1939-327X |
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| Abstract | Expansion of Human Regulatory T-Cells From Patients With Type 1 Diabetes
Amy L. Putnam 1 ,
Todd M. Brusko 1 ,
Michael R. Lee 1 ,
Weihong Liu 1 ,
Gregory L. Szot 1 ,
Taumoha Ghosh 1 ,
Mark A. Atkinson 2 and
Jeffrey A. Bluestone 1
1 Diabetes Center at the University of California, San Francisco (UCSF), San Francisco, California
2 Department of Pathology, University of Florida, College of Medicine, Gainesville, Florida
Corresponding author: Jeffrey A. Bluestone, jbluest{at}diabetes.ucsf.edu
Abstract
OBJECTIVE— Regulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal
models of autoimmunity to human clinical trials requires robust methods for the isolation and expansion of these cells—a need
forming the basis for these studies.
RESEARCH DESIGN AND METHODS— Tregs from recent-onset type 1 diabetic patients and healthy control subjects were isolated by fluorescence-activated cell
sorting and compared for their capacity to expand in vitro in response to anti-CD3–anti-CD28–coated microbeads and IL-2. Expanded
cells were examined for suppressive function, lineage markers and FOXP3, and cytokine production.
RESULTS— Both CD4 + CD127 lo/− and CD4 + CD127 lo/− CD25 + T-cells could be expanded and used as Tregs. However, expansion of CD4 + CD127 lo/− cells required the addition of rapamycin to maintain lineage purity. In contrast, expansion of CD4 + CD127 lo/− CD25 + T-cells, especially the CD45RA + subset, resulted in high yield, functional Tregs that maintained higher FOXP3 expression in the absence of rapamycin. Tregs
from type 1 diabetic patients and control subjects expanded similarly and were equally capable of suppressing T-cell proliferation.
Regulatory cytokines were produced by Tregs after culture; however, a portion of FOXP3 + cells were capable of producing interferon (IFN)-γ after reactivation. IFN-γ production was observed from both CD45RO + and CD45RA + Treg populations.
CONCLUSIONS— The results support the feasibility of isolating Tregs for in vitro expansion. Based on expansion capacity, FOXP3 stability,
and functional properties, the CD4 + CD127 lo/− CD25 + T-cells represent a viable cell population for cellular therapy in this autoimmune disease.
Footnotes
Published ahead of print at http://diabetes.diabetesjournals.org on 15 December 2008.
A.L.P. and T.M.B. contributed equally to this work.
Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work
is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Accepted December 5, 2008.
Received August 25, 2008.
DIABETES |
|---|---|
| AbstractList | OBJECTIVE--Regulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal models of autoimmunity to human clinical trials requires robust methods for the isolation and expansion of these cells--a need forming the basis for these studies. RESEARCH DESIGN AND METHODS--Tregs from recent-onset type 1 diabetic patients and healthy control subjects were isolated by fluorescence-activated cell sorting and compared for their capacity to expand in vitro in response to anti-CD3-antiCD28-coated microbeads and IL-2. Expanded cells were examined for suppressive function, lineage markers and FOXP3, and cytokine production. RESULTS--Both [CD4.sup.+][CD127.sup.lo/-] and [CD4.sup.+][CD127.sup.lo/-][CD25.sup.+] T-cells could be expanded and used as Tregs. However, expansion of [CD4.sup.+][CD127.sup.lo/-] cells required the addition of rapamycin to maintain lineage purity. In contrast, expansion of [CD4.sup.+][CD127.sup.lo/-][CD25.sup.+] T-cells, especially the [CD45RA.sup.+] subset, resulted in high yield, functional Tregs that maintained higher FOXP3 expression in the absence of rapamycin. Tregs from type 1 diabetic patients and control subjects expanded similarly and were equally capable of suppressing T-cell proliferation. Regulatory cytokines were produced by Tregs after culture; however, a portion of [FOXP3.sup.+] cells were capable of producing interferon (IFN)-γ after reactivation. IFN-γ production was observed from both [CD45RO.sup.+] and [CD45RA.sup.+] Treg populations. CONCLUSIONS--The results support the feasibility of isolating Tregs for in vitro expansion. Based on expansion capacity, FOXP3 stability, and functional properties, the [CD4.sup.+][CD127.sup.lo/-][CD25.sup.+] T-cells represent a viable cell population for cellular therapy in this autoimmune disease. Regulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal models of autoimmunity to human clinical trials requires robust methods for the isolation and expansion of these cells-a need forming the basis for these studies.OBJECTIVERegulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal models of autoimmunity to human clinical trials requires robust methods for the isolation and expansion of these cells-a need forming the basis for these studies.Tregs from recent-onset type 1 diabetic patients and healthy control subjects were isolated by fluorescence-activated cell sorting and compared for their capacity to expand in vitro in response to anti-CD3-anti-CD28-coated microbeads and IL-2. Expanded cells were examined for suppressive function, lineage markers and FOXP3, and cytokine production.RESEARCH DESIGN AND METHODSTregs from recent-onset type 1 diabetic patients and healthy control subjects were isolated by fluorescence-activated cell sorting and compared for their capacity to expand in vitro in response to anti-CD3-anti-CD28-coated microbeads and IL-2. Expanded cells were examined for suppressive function, lineage markers and FOXP3, and cytokine production.Both CD4+CD127(lo/-) and CD4+CD127(lo/-)CD25+ T-cells could be expanded and used as Tregs. However, expansion of CD4+CD127(lo/-) cells required the addition of rapamycin to maintain lineage purity. In contrast, expansion of CD4+CD127(lo/-)CD25+ T-cells, especially the CD45RA+ subset, resulted in high yield, functional Tregs that maintained higher FOXP3 expression in the absence of rapamycin. Tregs from type 1 diabetic patients and control subjects expanded similarly and were equally capable of suppressing T-cell proliferation. Regulatory cytokines were produced by Tregs after culture; however, a portion of FOXP3+ cells were capable of producing interferon (IFN)-gamma after reactivation. IFN-gamma production was observed from both CD45RO+ and CD45RA+ Treg populations.RESULTSBoth CD4+CD127(lo/-) and CD4+CD127(lo/-)CD25+ T-cells could be expanded and used as Tregs. However, expansion of CD4+CD127(lo/-) cells required the addition of rapamycin to maintain lineage purity. In contrast, expansion of CD4+CD127(lo/-)CD25+ T-cells, especially the CD45RA+ subset, resulted in high yield, functional Tregs that maintained higher FOXP3 expression in the absence of rapamycin. Tregs from type 1 diabetic patients and control subjects expanded similarly and were equally capable of suppressing T-cell proliferation. Regulatory cytokines were produced by Tregs after culture; however, a portion of FOXP3+ cells were capable of producing interferon (IFN)-gamma after reactivation. IFN-gamma production was observed from both CD45RO+ and CD45RA+ Treg populations.The results support the feasibility of isolating Tregs for in vitro expansion. Based on expansion capacity, FOXP3 stability, and functional properties, the CD4+CD127(lo/-)CD25+ T-cells represent a viable cell population for cellular therapy in this autoimmune disease.CONCLUSIONSThe results support the feasibility of isolating Tregs for in vitro expansion. Based on expansion capacity, FOXP3 stability, and functional properties, the CD4+CD127(lo/-)CD25+ T-cells represent a viable cell population for cellular therapy in this autoimmune disease. Regulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal models of autoimmunity to human clinical trials requires robust methods for the isolation and expansion of these cells-a need forming the basis for these studies. Tregs from recent-onset type 1 diabetic patients and healthy control subjects were isolated by fluorescence-activated cell sorting and compared for their capacity to expand in vitro in response to anti-CD3-anti-CD28-coated microbeads and IL-2. Expanded cells were examined for suppressive function, lineage markers and FOXP3, and cytokine production. Both CD4+CD127(lo/-) and CD4+CD127(lo/-)CD25+ T-cells could be expanded and used as Tregs. However, expansion of CD4+CD127(lo/-) cells required the addition of rapamycin to maintain lineage purity. In contrast, expansion of CD4+CD127(lo/-)CD25+ T-cells, especially the CD45RA+ subset, resulted in high yield, functional Tregs that maintained higher FOXP3 expression in the absence of rapamycin. Tregs from type 1 diabetic patients and control subjects expanded similarly and were equally capable of suppressing T-cell proliferation. Regulatory cytokines were produced by Tregs after culture; however, a portion of FOXP3+ cells were capable of producing interferon (IFN)-gamma after reactivation. IFN-gamma production was observed from both CD45RO+ and CD45RA+ Treg populations. The results support the feasibility of isolating Tregs for in vitro expansion. Based on expansion capacity, FOXP3 stability, and functional properties, the CD4+CD127(lo/-)CD25+ T-cells represent a viable cell population for cellular therapy in this autoimmune disease. Regulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal models of autoimmunity to human clinical trials requires robust methods for the isolation and expansion of these cells-a need forming the basis for these studies. Tregs from recent-onset type 1 diabetic patients and healthy control subjects were isolated by fluorescence-activated cell sorting and compared for their capacity to expand in vitro in response to anti-CD3-anti-CD28-coated microbeads and IL-2. Expanded cells were examined for suppressive function, lineage markers and FOXP3, and cytokine production. Both CD4+CD127(lo/-) and CD4+CD127(lo/-)CD25+ T-cells could be expanded and used as Tregs. However, expansion of CD4+CD127(lo/-) cells required the addition of rapamycin to maintain lineage purity. In contrast, expansion of CD4+CD127(lo/-)CD25+ T-cells, especially the CD45RA+ subset, resulted in high yield, functional Tregs that maintained higher FOXP3 expression in the absence of rapamycin. Tregs from type 1 diabetic patients and control subjects expanded similarly and were equally capable of suppressing T-cell proliferation. Regulatory cytokines were produced by Tregs after culture; however, a portion of FOXP3+ cells were capable of producing interferon (IFN)-gamma after reactivation. IFN-gamma production was observed from both CD45RO+ and CD45RA+ Treg populations. The results support the feasibility of isolating Tregs for in vitro expansion. Based on expansion capacity, FOXP3 stability, and functional properties, the CD4+CD127(lo/-)CD25+ T-cells represent a viable cell population for cellular therapy in this autoimmune disease. OBJECTIVE—Regulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal models of autoimmunity to human clinical trials requires robust methods for the isolation and expansion of these cells—a need forming the basis for these studies. RESEARCH DESIGN AND METHODS—Tregs from recent-onset type 1 diabetic patients and healthy control subjects were isolated by fluorescence-activated cell sorting and compared for their capacity to expand in vitro in response to anti-CD3–anti-CD28–coated microbeads and IL-2. Expanded cells were examined for suppressive function, lineage markers and FOXP3, and cytokine production. RESULTS—Both CD4+CD127lo/− and CD4+CD127lo/−CD25+ T-cells could be expanded and used as Tregs. However, expansion of CD4+CD127lo/− cells required the addition of rapamycin to maintain lineage purity. In contrast, expansion of CD4+CD127lo/−CD25+ T-cells, especially the CD45RA+ subset, resulted in high yield, functional Tregs that maintained higher FOXP3 expression in the absence of rapamycin. Tregs from type 1 diabetic patients and control subjects expanded similarly and were equally capable of suppressing T-cell proliferation. Regulatory cytokines were produced by Tregs after culture; however, a portion of FOXP3+ cells were capable of producing interferon (IFN)-γ after reactivation. IFN-γ production was observed from both CD45RO+ and CD45RA+ Treg populations. CONCLUSIONS—The results support the feasibility of isolating Tregs for in vitro expansion. Based on expansion capacity, FOXP3 stability, and functional properties, the CD4+CD127lo/−CD25+ T-cells represent a viable cell population for cellular therapy in this autoimmune disease. Expansion of Human Regulatory T-Cells From Patients With Type 1 Diabetes Amy L. Putnam 1 , Todd M. Brusko 1 , Michael R. Lee 1 , Weihong Liu 1 , Gregory L. Szot 1 , Taumoha Ghosh 1 , Mark A. Atkinson 2 and Jeffrey A. Bluestone 1 1 Diabetes Center at the University of California, San Francisco (UCSF), San Francisco, California 2 Department of Pathology, University of Florida, College of Medicine, Gainesville, Florida Corresponding author: Jeffrey A. Bluestone, jbluest{at}diabetes.ucsf.edu Abstract OBJECTIVE— Regulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal models of autoimmunity to human clinical trials requires robust methods for the isolation and expansion of these cells—a need forming the basis for these studies. RESEARCH DESIGN AND METHODS— Tregs from recent-onset type 1 diabetic patients and healthy control subjects were isolated by fluorescence-activated cell sorting and compared for their capacity to expand in vitro in response to anti-CD3–anti-CD28–coated microbeads and IL-2. Expanded cells were examined for suppressive function, lineage markers and FOXP3, and cytokine production. RESULTS— Both CD4 + CD127 lo/− and CD4 + CD127 lo/− CD25 + T-cells could be expanded and used as Tregs. However, expansion of CD4 + CD127 lo/− cells required the addition of rapamycin to maintain lineage purity. In contrast, expansion of CD4 + CD127 lo/− CD25 + T-cells, especially the CD45RA + subset, resulted in high yield, functional Tregs that maintained higher FOXP3 expression in the absence of rapamycin. Tregs from type 1 diabetic patients and control subjects expanded similarly and were equally capable of suppressing T-cell proliferation. Regulatory cytokines were produced by Tregs after culture; however, a portion of FOXP3 + cells were capable of producing interferon (IFN)-γ after reactivation. IFN-γ production was observed from both CD45RO + and CD45RA + Treg populations. CONCLUSIONS— The results support the feasibility of isolating Tregs for in vitro expansion. Based on expansion capacity, FOXP3 stability, and functional properties, the CD4 + CD127 lo/− CD25 + T-cells represent a viable cell population for cellular therapy in this autoimmune disease. Footnotes Published ahead of print at http://diabetes.diabetesjournals.org on 15 December 2008. A.L.P. and T.M.B. contributed equally to this work. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Accepted December 5, 2008. Received August 25, 2008. DIABETES OBJECTIVE—Regulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal models of autoimmunity to human clinical trials requires robust methods for the isolation and expansion of these cells—a need forming the basis for these studies. RESEARCH DESIGN AND METHODS—Tregs from recent-onset type 1 diabetic patients and healthy control subjects were isolated by fluorescence-activated cell sorting and compared for their capacity to expand in vitro in response to anti-CD3–anti-CD28–coated microbeads and IL-2. Expanded cells were examined for suppressive function, lineage markers and FOXP3, and cytokine production. RESULTS—Both CD4+CD127lo/− and CD4+CD127lo/−CD25+ T-cells could be expanded and used as Tregs. However, expansion of CD4+CD127lo/− cells required the addition of rapamycin to maintain lineage purity. In contrast, expansion of CD4+CD127lo/−CD25+ T-cells, especially the CD45RA+ subset, resulted in high yield, functional Tregs that maintained higher FOXP3 expression in the absence of rapamycin. Tregs from type 1 diabetic patients and control subjects expanded similarly and were equally capable of suppressing T-cell proliferation. Regulatory cytokines were produced by Tregs after culture; however, a portion of FOXP3+ cells were capable of producing interferon (IFN)-γ after reactivation. IFN-γ production was observed from both CD45RO+ and CD45RA+ Treg populations. CONCLUSIONS—The results support the feasibility of isolating Tregs for in vitro expansion. Based on expansion capacity, FOXP3 stability, and functional properties, the CD4+CD127lo/−CD25+ T-cells represent a viable cell population for cellular therapy in this autoimmune disease. |
| Audience | Professional |
| Author | Amy L. Putnam Weihong Liu Jeffrey A. Bluestone Todd M. Brusko Mark A. Atkinson Taumoha Ghosh Gregory L. Szot Michael R. Lee |
| AuthorAffiliation | 2 Department of Pathology, University of Florida, College of Medicine, Gainesville, Florida 1 Diabetes Center at the University of California, San Francisco (UCSF), San Francisco, California |
| AuthorAffiliation_xml | – name: 1 Diabetes Center at the University of California, San Francisco (UCSF), San Francisco, California – name: 2 Department of Pathology, University of Florida, College of Medicine, Gainesville, Florida |
| Author_xml | – sequence: 1 givenname: Amy L. surname: Putnam fullname: Putnam, Amy L. organization: Diabetes Center at the University of California, San Francisco (UCSF), San Francisco, California – sequence: 2 givenname: Todd M. surname: Brusko fullname: Brusko, Todd M. organization: Diabetes Center at the University of California, San Francisco (UCSF), San Francisco, California – sequence: 3 givenname: Michael R. surname: Lee fullname: Lee, Michael R. organization: Diabetes Center at the University of California, San Francisco (UCSF), San Francisco, California – sequence: 4 givenname: Weihong surname: Liu fullname: Liu, Weihong organization: Diabetes Center at the University of California, San Francisco (UCSF), San Francisco, California – sequence: 5 givenname: Gregory L. surname: Szot fullname: Szot, Gregory L. organization: Diabetes Center at the University of California, San Francisco (UCSF), San Francisco, California – sequence: 6 givenname: Taumoha surname: Ghosh fullname: Ghosh, Taumoha organization: Diabetes Center at the University of California, San Francisco (UCSF), San Francisco, California – sequence: 7 givenname: Mark A. surname: Atkinson fullname: Atkinson, Mark A. organization: Department of Pathology, University of Florida, College of Medicine, Gainesville, Florida – sequence: 8 givenname: Jeffrey A. surname: Bluestone fullname: Bluestone, Jeffrey A. organization: Diabetes Center at the University of California, San Francisco (UCSF), San Francisco, California |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19074986$$D View this record in MEDLINE/PubMed |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Corresponding author: Jeffrey A. Bluestone, jbluest@diabetes.ucsf.edu Published ahead of print at http://diabetes.diabetesjournals.org on 15 December 2008. A.L.P. and T.M.B. contributed equally to this work. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. |
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| Snippet | Expansion of Human Regulatory T-Cells From Patients With Type 1 Diabetes
Amy L. Putnam 1 ,
Todd M. Brusko 1 ,
Michael R. Lee 1 ,
Weihong Liu 1 ,
Gregory L.... OBJECTIVE—Regulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal models of... Regulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal models of autoimmunity to human... OBJECTIVE--Regulatory T-cells (Tregs) have catalyzed the field of immune regulation. However, translating Treg-based therapies from animal models of... |
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| StartPage | 652 |
| SubjectTerms | Adult Age of Onset Antigens, CD - immunology Autoimmune diseases Autoimmunity CD4-Positive T-Lymphocytes - immunology Cell Division Cell Proliferation Cells Cytokines - metabolism Diabetes Diabetes Mellitus, Type 1 - immunology Disease Female Flow Cytometry Forkhead Transcription Factors - analysis Health aspects Humans Immunology and Transplantation Immunosuppression Ionomycin - pharmacology Male Phenotype Reference Values Research design T cells T-Lymphocytes, Regulatory - cytology T-Lymphocytes, Regulatory - drug effects T-Lymphocytes, Regulatory - immunology Tetradecanoylphorbol Acetate - pharmacology Type 1 diabetes Young Adult |
| Title | Expansion of Human Regulatory T-Cells From Patients With Type 1 Diabetes |
| URI | http://diabetes.diabetesjournals.org/content/58/3/652.abstract https://www.ncbi.nlm.nih.gov/pubmed/19074986 https://www.proquest.com/docview/216470353 https://www.proquest.com/docview/66976361 https://pubmed.ncbi.nlm.nih.gov/PMC2646064 |
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