Secretory phospholipase A2-IID is an effector molecule of CD4⁺CD25⁺ regulatory T cells

Suppression by natural CD4⁺CD25⁺ regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate suppression is not well understood. Here, we show that secreted phospholipase A2 (sPLA2)-IID is selectively produced by Tregs. sPLA2-IID is a potent...

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Published inProceedings of the National Academy of Sciences - PNAS Vol. 106; no. 28; pp. 11673 - 11678
Main Authors von Allmen, Caroline E, Schmitz, Nicole, Bauer, Monika, Hinton, Heather J, Kurrer, Michael O, Buser, Regula B, Gwerder, Myriam, Muntwiler, Simone, Sparwasser, Tim, Beerli, Roger R, Bachmann, Martin F
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences 14.07.2009
National Acad Sciences
Subjects
Adoptive Transfer
Animals
Antibodies
Antigen presenting cells
Autoimmune diseases
Biological Sciences
Catalytic activity
Cell Differentiation - drug effects
Cell Differentiation - immunology
Cell Proliferation - drug effects
Cells
Colitis
Colitis - immunology
Colitis - prevention & control
Complementary DNA
Disease models
DNA Primers - genetics
Flow Cytometry
Group II Phospholipases A2 - metabolism
Group II Phospholipases A2 - pharmacology
Inflammatory bowel disease
Mice
Molecules
Multiple sclerosis
Multiple Sclerosis - immunology
Multiple Sclerosis - prevention & control
Proteins
Receptors
Recombinant Fusion Proteins - pharmacology
Reverse Transcriptase Polymerase Chain Reaction
Rodents
Signal transduction
Signal Transduction - immunology
T lymphocytes
T-Lymphocytes, Regulatory - metabolism
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Abstract Suppression by natural CD4⁺CD25⁺ regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate suppression is not well understood. Here, we show that secreted phospholipase A2 (sPLA2)-IID is selectively produced by Tregs. sPLA2-IID is a potent mediator of Treg function, because it strongly suppressed proliferation of CD4⁺ and CD8⁺ T cells in vitro and in vivo in a manner independent of its catalytic activity. Furthermore, sPLA2-IID promoted the differentiation of Tregs, presumably via attenuating signaling through the PI3K/Akt/mammalian target of rapamycin pathway. Importantly, administration of a sPLA2-IID-Fc fusion protein inhibited disease development in murine models of colitis and multiple sclerosis, suggesting that sPLA2-IID's immunosuppressive function might be exploited therapeutically.
AbstractList Suppression by natural CD4(+)CD25(+) regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate suppression is not well understood. Here, we show that secreted phospholipase A2 (sPLA2)-IID is selectively produced by Tregs. sPLA2-IID is a potent mediator of Treg function, because it strongly suppressed proliferation of CD4(+) and CD8(+) T cells in vitro and in vivo in a manner independent of its catalytic activity. Furthermore, sPLA2-IID promoted the differentiation of Tregs, presumably via attenuating signaling through the PI3K/Akt/mammalian target of rapamycin pathway. Importantly, administration of a sPLA2-IID-Fc fusion protein inhibited disease development in murine models of colitis and multiple sclerosis, suggesting that sPLA2-IID's immunosuppressive function might be exploited therapeutically.
Suppression by natural CD4 + CD25 + regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate suppression is not well understood. Here, we show that secreted phospholipase A2 (sPLA2)-IID is selectively produced by Tregs. sPLA2-IID is a potent mediator of Treg function, because it strongly suppressed proliferation of CD4 + and CD8 + T cells in vitro and in vivo in a manner independent of its catalytic activity. Furthermore, sPLA2-IID promoted the differentiation of Tregs, presumably via attenuating signaling through the PI3K/Akt/mammalian target of rapamycin pathway. Importantly, administration of a sPLA2-IID-Fc fusion protein inhibited disease development in murine models of colitis and multiple sclerosis, suggesting that sPLA2-IID's immunosuppressive function might be exploited therapeutically.
Suppression by natural CD4⁺CD25⁺ regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate suppression is not well understood. Here, we show that secreted phospholipase A2 (sPLA2)-IID is selectively produced by Tregs. sPLA2-IID is a potent mediator of Treg function, because it strongly suppressed proliferation of CD4⁺ and CD8⁺ T cells in vitro and in vivo in a manner independent of its catalytic activity. Furthermore, sPLA2-IID promoted the differentiation of Tregs, presumably via attenuating signaling through the PI3K/Akt/mammalian target of rapamycin pathway. Importantly, administration of a sPLA2-IID-Fc fusion protein inhibited disease development in murine models of colitis and multiple sclerosis, suggesting that sPLA2-IID's immunosuppressive function might be exploited therapeutically.
Suppression by natural CD4...CD25... regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate suppression is not well understood. Here, we show that secreted phospholipase A2 (sPLA2)-IID is selectively produced by Tregs. sPLA2-IID is a potent mediator of Treg function, because it strongly suppressed proliferation of CD4... and CD8... T cells in vitro and in vivo in a manner independent of its catalytic activity. Furthermore, sPLA2-IID promoted the differentiation of Tregs, presumably via attenuating signaling through the PI3K/Akt/mammalian target of rapamycin pathway. Importantly, administration of a sPLA2-IID-Fc fusion protein inhibited disease development in murine models of colitis and multiple sclerosis, suggesting that sPLA2-IID's immunosuppressive function might be exploited therapeutically. (ProQuest: ... denotes formulae/symbols omitted.)
Suppression by natural CD4⁺ CD25⁺ regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate suppression is not well understood. Here, we show that secreted phospholipase A2 (sPLA2)-IID is selectively produced by Tregs. sPLA2-IID is a potent mediator of Treg function, because it strongly suppressed proliferation of CD4⁺ and CD8⁺ T cells in vitro and in vivo in a manner independent of its catalytic activity. Furthermore, sPLA2-IID promoted the differentiation of Tregs, presumably via attenuating signaling through the PI3K/Akt/mammalian target of rapamycin pathway. Importantly, administration of a sPLA2-IID-Fc fusion protein inhibited disease development in murine models of colitis and multiple sclerosis, suggesting that sPLA2-IID's immunosuppressive function might be exploited therapeutically.
Author von Allmen, Caroline E
Sparwasser, Tim
Kurrer, Michael O
Hinton, Heather J
Buser, Regula B
Muntwiler, Simone
Bachmann, Martin F
Bauer, Monika
Schmitz, Nicole
Beerli, Roger R
Gwerder, Myriam
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  fullname: Sparwasser, Tim
– sequence: 10
  fullname: Beerli, Roger R
– sequence: 11
  fullname: Bachmann, Martin F
BackLink https://www.ncbi.nlm.nih.gov/pubmed/19564598$$D View this record in MEDLINE/PubMed
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Edited by Dan R. Littman, New York University Medical Center, New York, NY, and approved May 4, 2009
Author contributions: C.E.v.A., N.S., H.J.H., R.R.B., and M.F.B. designed research; C.E.v.A., N.S., M.B., M.O.K., R.B.B., M.G., S.M., and R.R.B. performed research; T.S. contributed new reagents/analytic tools; C.E.v.A., N.S., R.R.B., and M.F.B. analyzed data; and C.E.v.A., R.R.B., and M.F.B. wrote the paper.
1R.R.B. and M.F.B. contributed equally to this work.
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Snippet Suppression by natural CD4⁺CD25⁺ regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate...
Suppression by natural CD4⁺ CD25⁺ regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate...
Suppression by natural CD4 + CD25 + regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate...
Suppression by natural CD4(+)CD25(+) regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate...
Suppression by natural CD4 + CD25 + regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate...
Suppression by natural CD4...CD25... regulatory T cells (Tregs) is one mechanism by which tolerance is maintained. However, the way in which Tregs mediate...
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StartPage 11673
SubjectTerms Adoptive Transfer
Animals
Antibodies
Antigen presenting cells
Autoimmune diseases
Biological Sciences
Catalytic activity
Cell Differentiation - drug effects
Cell Differentiation - immunology
Cell Proliferation - drug effects
Cells
Colitis
Colitis - immunology
Colitis - prevention & control
Complementary DNA
Disease models
DNA Primers - genetics
Flow Cytometry
Group II Phospholipases A2 - metabolism
Group II Phospholipases A2 - pharmacology
Inflammatory bowel disease
Mice
Molecules
Multiple sclerosis
Multiple Sclerosis - immunology
Multiple Sclerosis - prevention & control
Proteins
Receptors
Recombinant Fusion Proteins - pharmacology
Reverse Transcriptase Polymerase Chain Reaction
Rodents
Signal transduction
Signal Transduction - immunology
T lymphocytes
T-Lymphocytes, Regulatory - metabolism
Title Secretory phospholipase A2-IID is an effector molecule of CD4⁺CD25⁺ regulatory T cells
URI https://www.jstor.org/stable/40484009
http://www.pnas.org/content/106/28/11673.abstract
https://www.ncbi.nlm.nih.gov/pubmed/19564598
https://www.proquest.com/docview/201417225/abstract/
https://search.proquest.com/docview/67501806
https://pubmed.ncbi.nlm.nih.gov/PMC2710677
Volume 106
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