Homogeneous Expansion of Human T-Regulatory Cells Via Tumor Necrosis Factor Receptor 2

T-regulatory cells (T regs ) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease, autoimmunity and asthma. Clinical applications of T regs have not been fully realized because standard methods of expansion ex vivo produce heterogeneous...

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Vydáno v:Scientific reports Ročník 3; číslo 1; s. 3153
Hlavní autoři: Okubo, Yoshiaki, Mera, Toshiyuki, Wang, Limei, Faustman, Denise L.
Médium: Journal Article
Jazyk:angličtina
Vydáno: London Nature Publishing Group UK 06.11.2013
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ISSN:2045-2322, 2045-2322
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Abstract T-regulatory cells (T regs ) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease, autoimmunity and asthma. Clinical applications of T regs have not been fully realized because standard methods of expansion ex vivo produce heterogeneous progeny consisting of mixed populations of CD4 + T cells. Heterogeneous progeny are risky for human clinical trials and face significant regulatory hurdles. With the goal of producing homogeneous T regs , we developed a novel expansion protocol targeting tumor necrosis factor receptors (TNFR) on T regs . In in vitro studies, a TNFR2 agonist was found superior to standard methods in proliferating human T regs into a phenotypically homogeneous population consisting of 14 cell surface markers. The TNFR2 agonist-expanded T regs also were functionally superior in suppressing a key T reg target cell, cytotoxic T-lymphocytes. Targeting the TNFR2 receptor during ex vivo expansion is a new means for producing homogeneous and potent human T regs for clinical opportunities.
AbstractList T-regulatory cells (T regs ) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease, autoimmunity and asthma. Clinical applications of T regs have not been fully realized because standard methods of expansion ex vivo produce heterogeneous progeny consisting of mixed populations of CD4 + T cells. Heterogeneous progeny are risky for human clinical trials and face significant regulatory hurdles. With the goal of producing homogeneous T regs , we developed a novel expansion protocol targeting tumor necrosis factor receptors (TNFR) on T regs . In in vitro studies, a TNFR2 agonist was found superior to standard methods in proliferating human T regs into a phenotypically homogeneous population consisting of 14 cell surface markers. The TNFR2 agonist-expanded T regs also were functionally superior in suppressing a key T reg target cell, cytotoxic T-lymphocytes. Targeting the TNFR2 receptor during ex vivo expansion is a new means for producing homogeneous and potent human T regs for clinical opportunities.
T-regulatory cells (T(regs)) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease, autoimmunity, and asthma. Clinical applications of T(regs) have not been fully realized because standard methods of expansion ex vivo produce heterogeneous progeny consisting of mixed populations of CD4 + T cells. Heterogeneous progeny are risky for human clinical trials and face significant regulatory hurdles. With the goal of producing homogeneous T(regs), we developed a novel expansion protocol targeting tumor necrosis factor receptors (TNFR) on T(regs). In in vitro studies, a TNFR2 agonist was found superior to standard methods in proliferating human T(regs) into a phenotypically homogeneous population consisting of 14 cell surface markers. The TNFR2 agonist-expanded T(regs) also were functionally superior in suppressing a key T(reg) target cell, cytotoxic T-lymphocytes. Targeting the TNFR2 receptor during ex vivo expansion is a new means for producing homogeneous and potent human T(regs) for clinical opportunities.
T-regulatory cells (T(regs)) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease, autoimmunity, and asthma. Clinical applications of T(regs) have not been fully realized because standard methods of expansion ex vivo produce heterogeneous progeny consisting of mixed populations of CD4 + T cells. Heterogeneous progeny are risky for human clinical trials and face significant regulatory hurdles. With the goal of producing homogeneous T(regs), we developed a novel expansion protocol targeting tumor necrosis factor receptors (TNFR) on T(regs). In in vitro studies, a TNFR2 agonist was found superior to standard methods in proliferating human T(regs) into a phenotypically homogeneous population consisting of 14 cell surface markers. The TNFR2 agonist-expanded T(regs) also were functionally superior in suppressing a key T(reg) target cell, cytotoxic T-lymphocytes. Targeting the TNFR2 receptor during ex vivo expansion is a new means for producing homogeneous and potent human T(regs) for clinical opportunities.T-regulatory cells (T(regs)) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease, autoimmunity, and asthma. Clinical applications of T(regs) have not been fully realized because standard methods of expansion ex vivo produce heterogeneous progeny consisting of mixed populations of CD4 + T cells. Heterogeneous progeny are risky for human clinical trials and face significant regulatory hurdles. With the goal of producing homogeneous T(regs), we developed a novel expansion protocol targeting tumor necrosis factor receptors (TNFR) on T(regs). In in vitro studies, a TNFR2 agonist was found superior to standard methods in proliferating human T(regs) into a phenotypically homogeneous population consisting of 14 cell surface markers. The TNFR2 agonist-expanded T(regs) also were functionally superior in suppressing a key T(reg) target cell, cytotoxic T-lymphocytes. Targeting the TNFR2 receptor during ex vivo expansion is a new means for producing homogeneous and potent human T(regs) for clinical opportunities.
T-regulatory cells (Tregs) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease, autoimmunity, and asthma. Clinical applications of Tregs have not been fully realized because standard methods of expansion ex vivo produce heterogeneous progeny consisting of mixed populations of CD4 + T cells. Heterogeneous progeny are risky for human clinical trials and face significant regulatory hurdles. With the goal of producing homogeneous Tregs, we developed a novel expansion protocol targeting tumor necrosis factor receptors (TNFR) on Tregs. In in vitro studies, a TNFR2 agonist was found superior to standard methods in proliferating human Tregs into a phenotypically homogeneous population consisting of 14 cell surface markers. The TNFR2 agonist-expanded Tregs also were functionally superior in suppressing a key Treg target cell, cytotoxic T-lymphocytes. Targeting the TNFR2 receptor during ex vivo expansion is a new means for producing homogeneous and potent human Tregs for clinical opportunities.
ArticleNumber 3153
Author Mera, Toshiyuki
Faustman, Denise L.
Okubo, Yoshiaki
Wang, Limei
Author_xml – sequence: 1
  givenname: Yoshiaki
  surname: Okubo
  fullname: Okubo, Yoshiaki
  organization: Immunobiology Laboratory, Massachusetts General Hospital and Harvard Medical School
– sequence: 2
  givenname: Toshiyuki
  surname: Mera
  fullname: Mera, Toshiyuki
  organization: Immunobiology Laboratory, Massachusetts General Hospital and Harvard Medical School
– sequence: 3
  givenname: Limei
  surname: Wang
  fullname: Wang, Limei
  organization: Immunobiology Laboratory, Massachusetts General Hospital and Harvard Medical School
– sequence: 4
  givenname: Denise L.
  surname: Faustman
  fullname: Faustman, Denise L.
  organization: Immunobiology Laboratory, Massachusetts General Hospital and Harvard Medical School
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24193319$$D View this record in MEDLINE/PubMed
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Snippet T-regulatory cells (T regs ) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease, autoimmunity...
T-regulatory cells (T(regs)) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease,...
T-regulatory cells (Tregs ) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease, autoimmunity,...
T-regulatory cells (Tregs) are a rare lymphocyte subtype that shows promise for treating infectious disease, allergy, graft-versus-host disease, autoimmunity,...
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StartPage 3153
SubjectTerms 13
13/1
631/1647/664/1364
631/61/24
692/308/575
Allergies
Animals
Antibodies, Monoclonal - immunology
Asthma
Autoimmune diseases
Autoimmunity
CD4 antigen
CD4-Positive T-Lymphocytes - cytology
CD4-Positive T-Lymphocytes - drug effects
CD4-Positive T-Lymphocytes - metabolism
Cell Proliferation
Cell surface
Cells, Cultured
Clinical trials
Cytokines - metabolism
Cytotoxicity
Forkhead Transcription Factors - metabolism
Graft-versus-host reaction
Humanities and Social Sciences
Humans
Immunoregulation
Infectious diseases
Interleukin-2 - genetics
Interleukin-2 - metabolism
Interleukin-2 - pharmacology
Lymphocytes
Lymphocytes T
multidisciplinary
Necrosis
Offspring
Receptors, Tumor Necrosis Factor, Type II - agonists
Receptors, Tumor Necrosis Factor, Type II - antagonists & inhibitors
Receptors, Tumor Necrosis Factor, Type II - metabolism
Recombinant Proteins - biosynthesis
Recombinant Proteins - genetics
Recombinant Proteins - pharmacology
Science
Surface markers
T cell receptors
T-Lymphocytes, Regulatory - cytology
T-Lymphocytes, Regulatory - drug effects
T-Lymphocytes, Regulatory - metabolism
Therapeutic applications
Tumor necrosis factor
Tumor necrosis factor receptor 2
Tumor necrosis factor receptors
Tumor Necrosis Factor-alpha - genetics
Tumor Necrosis Factor-alpha - metabolism
Tumor Necrosis Factor-alpha - pharmacology
Tumor necrosis factor-TNF
Title Homogeneous Expansion of Human T-Regulatory Cells Via Tumor Necrosis Factor Receptor 2
URI https://link.springer.com/article/10.1038/srep03153
https://www.ncbi.nlm.nih.gov/pubmed/24193319
https://www.proquest.com/docview/1898207688
https://www.proquest.com/docview/1449268720
https://pubmed.ncbi.nlm.nih.gov/PMC3818650
Volume 3
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