Transplant Tolerance to Pancreatic Islets Is Initiated in the Graft and Sustained in the Spleen
Identifieur interne : 001B73 ( PascalFrancis/Corpus ); précédent : 001B72; suivant : 001B74Transplant Tolerance to Pancreatic Islets Is Initiated in the Graft and Sustained in the Spleen
Auteurs : N. Gagliani ; T. Jofra ; A. Valle ; A. Stabilini ; C. Morsiani ; S. Gregori ; S. Deng ; D. M. Rothstein ; M. Atkinson ; M. Kamanaka ; R. A. Flavell ; M. G. Roncarolo ; M. BattagliaSource :
- American journal of transplantation : (Print) [ 1600-6135 ] ; 2013.
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English descriptors
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Abstract
The immune system is comprised of several CD4+ T regulatory (Treg) cell types, of which two, the Foxp3+ Treg and T regulatory type 1 (Tr1) cells, have frequently been associated with transplant tolerance. However, whether and how these two Treg-cell types synergize to promote allograft tolerance remains unknown. We previously developed a mouse model of allogeneic transplantation in which a specific immunomodulatory treatment leads to transplant tolerance through both Foxp3+ Treg and Tr1 cells. Here, we show that Foxp3+ Treg cells exert their regulatory function within the allograft and initiate engraftment locally and in a non-antigen (Ag) specific manner. Whereas CD4+CD25- T cells, which contain Tr1 cells, act from the spleen and are key to the maintenance of long-term tolerance. Importantly, the role of Foxp3+ Treg and Tr1 cells is not redundant once they are simultaneously expanded/induced in the same host. Moreover, our data show that long-term tolerance induced by Foxp3+ Treg-cell transfer is sustained by splenic Tr1 cells and functionally moves from the allograft to the spleen.
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Format Inist (serveur)
| NO : | PASCAL 13-0285793 INIST |
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| ET : | Transplant Tolerance to Pancreatic Islets Is Initiated in the Graft and Sustained in the Spleen |
| AU : | GAGLIANI (N.); JOFRA (T.); VALLE (A.); STABILINI (A.); MORSIANI (C.); GREGORI (S.); DENG (S.); ROTHSTEIN (D. M.); ATKINSON (M.); KAMANAKA (M.); FLAVELL (R. A.); RONCAROLO (M. G.); BATTAGLIA (M.) |
| AF : | San Raffaele Scientific Institute, Diabetes Research Institute/Milan/Italie (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 13 aut.); San Raffaele Telethon Institute for Gene Therapy/Milan/Italie (1 aut., 6 aut., 12 aut.); Vita-Salute San Raffaele University/Milan/Italie (1 aut., 12 aut.); Department of Medicine, Yale University School of Medicine/New Haven, CT/Etats-Unis (7 aut.); Starzl Transplantation Institute, University of Pittsburgh Medical Center/Pittsburgh, PA/Etats-Unis (8 aut.); Department of Pathology, The University of Florida/Gainesville, FL/Etats-Unis (9 aut.); Department of Immunobiology, Yale University School of Medicine/New Haven, CT/Etats-Unis (10 aut., 11 aut.); Howard Hughes Medical Institute/New Haven, CT/Etats-Unis (11 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | American journal of transplantation : (Print); ISSN 1600-6135; Etats-Unis; Da. 2013; Vol. 13; No. 8; Pp. 1963-1975; Bibl. 33 ref. |
| LA : | Anglais |
| EA : | The immune system is comprised of several CD4+ T regulatory (Treg) cell types, of which two, the Foxp3+ Treg and T regulatory type 1 (Tr1) cells, have frequently been associated with transplant tolerance. However, whether and how these two Treg-cell types synergize to promote allograft tolerance remains unknown. We previously developed a mouse model of allogeneic transplantation in which a specific immunomodulatory treatment leads to transplant tolerance through both Foxp3+ Treg and Tr1 cells. Here, we show that Foxp3+ Treg cells exert their regulatory function within the allograft and initiate engraftment locally and in a non-antigen (Ag) specific manner. Whereas CD4+CD25- T cells, which contain Tr1 cells, act from the spleen and are key to the maintenance of long-term tolerance. Importantly, the role of Foxp3+ Treg and Tr1 cells is not redundant once they are simultaneously expanded/induced in the same host. Moreover, our data show that long-term tolerance induced by Foxp3+ Treg-cell transfer is sustained by splenic Tr1 cells and functionally moves from the allograft to the spleen. |
| CC : | 002B25 |
| FD : | Greffe; Tolérance immune; Transplantation; Traitement; Ilot Langerhans; Rate; Chirurgie; Lymphocyte T régulateur |
| FG : | Pancréas endocrine |
| ED : | Graft; Immune tolerance; Transplantation; Treatment; Langerhans islet; Spleen; Surgery; T regulatory cell |
| EG : | Endocrine pancreas |
| SD : | Injerto; Tolerancia inmune; Trasplantación; Tratamiento; Isla Langerhans; Bazo; Cirugía; Lifocito T regulador |
| LO : | INIST-27587.354000501930860060 |
| ID : | 13-0285793 |
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Atkinson</name><affiliation><inist:fA14 i1="06"><s1>Department of Pathology, The University of Florida</s1><s2>Gainesville, FL</s2><s3>USA</s3><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Kamanaka, M" sort="Kamanaka, M" uniqKey="Kamanaka M" first="M." last="Kamanaka">M. Kamanaka</name><affiliation><inist:fA14 i1="07"><s1>Department of Immunobiology, Yale University School of Medicine</s1><s2>New Haven, CT</s2><s3>USA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Flavell, R A" sort="Flavell, R A" uniqKey="Flavell R" first="R. A." last="Flavell">R. A. Flavell</name><affiliation><inist:fA14 i1="07"><s1>Department of Immunobiology, Yale University School of Medicine</s1><s2>New Haven, CT</s2><s3>USA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="08"><s1>Howard Hughes Medical Institute</s1><s2>New Haven, CT</s2><s3>USA</s3><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Roncarolo, M G" sort="Roncarolo, M G" uniqKey="Roncarolo M" first="M. G." last="Roncarolo">M. G. Roncarolo</name><affiliation><inist:fA14 i1="02"><s1>San Raffaele Telethon Institute for Gene Therapy</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>6 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Vita-Salute San Raffaele University</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Battaglia, M" sort="Battaglia, M" uniqKey="Battaglia M" first="M." last="Battaglia">M. Battaglia</name><affiliation><inist:fA14 i1="01"><s1>San Raffaele Scientific Institute, Diabetes Research Institute</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">13-0285793</idno><date when="2013">2013</date><idno type="stanalyst">PASCAL 13-0285793 INIST</idno><idno type="RBID">Pascal:13-0285793</idno><idno type="wicri:Area/PascalFrancis/Corpus">001B73</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Transplant Tolerance to Pancreatic Islets Is Initiated in the Graft and Sustained in the Spleen</title><author><name sortKey="Gagliani, N" sort="Gagliani, N" uniqKey="Gagliani N" first="N." last="Gagliani">N. Gagliani</name><affiliation><inist:fA14 i1="01"><s1>San Raffaele Scientific Institute, Diabetes Research Institute</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>San Raffaele Telethon Institute for Gene Therapy</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>6 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Vita-Salute San Raffaele University</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Jofra, T" sort="Jofra, T" uniqKey="Jofra T" first="T." last="Jofra">T. Jofra</name><affiliation><inist:fA14 i1="01"><s1>San Raffaele Scientific Institute, Diabetes Research Institute</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Valle, A" sort="Valle, A" uniqKey="Valle A" first="A." last="Valle">A. Valle</name><affiliation><inist:fA14 i1="01"><s1>San Raffaele Scientific Institute, Diabetes Research Institute</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Stabilini, A" sort="Stabilini, A" uniqKey="Stabilini A" first="A." last="Stabilini">A. Stabilini</name><affiliation><inist:fA14 i1="01"><s1>San Raffaele Scientific Institute, Diabetes Research Institute</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Morsiani, C" sort="Morsiani, C" uniqKey="Morsiani C" first="C." last="Morsiani">C. Morsiani</name><affiliation><inist:fA14 i1="01"><s1>San Raffaele Scientific Institute, Diabetes Research Institute</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Gregori, S" sort="Gregori, S" uniqKey="Gregori S" first="S." last="Gregori">S. Gregori</name><affiliation><inist:fA14 i1="02"><s1>San Raffaele Telethon Institute for Gene Therapy</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>6 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Deng, S" sort="Deng, S" uniqKey="Deng S" first="S." last="Deng">S. Deng</name><affiliation><inist:fA14 i1="04"><s1>Department of Medicine, Yale University School of Medicine</s1><s2>New Haven, CT</s2><s3>USA</s3><sZ>7 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Rothstein, D M" sort="Rothstein, D M" uniqKey="Rothstein D" first="D. M." last="Rothstein">D. M. Rothstein</name><affiliation><inist:fA14 i1="05"><s1>Starzl Transplantation Institute, University of Pittsburgh Medical Center</s1><s2>Pittsburgh, PA</s2><s3>USA</s3><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Atkinson, M" sort="Atkinson, M" uniqKey="Atkinson M" first="M." last="Atkinson">M. Atkinson</name><affiliation><inist:fA14 i1="06"><s1>Department of Pathology, The University of Florida</s1><s2>Gainesville, FL</s2><s3>USA</s3><sZ>9 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Kamanaka, M" sort="Kamanaka, M" uniqKey="Kamanaka M" first="M." last="Kamanaka">M. Kamanaka</name><affiliation><inist:fA14 i1="07"><s1>Department of Immunobiology, Yale University School of Medicine</s1><s2>New Haven, CT</s2><s3>USA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Flavell, R A" sort="Flavell, R A" uniqKey="Flavell R" first="R. A." last="Flavell">R. A. Flavell</name><affiliation><inist:fA14 i1="07"><s1>Department of Immunobiology, Yale University School of Medicine</s1><s2>New Haven, CT</s2><s3>USA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="08"><s1>Howard Hughes Medical Institute</s1><s2>New Haven, CT</s2><s3>USA</s3><sZ>11 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Roncarolo, M G" sort="Roncarolo, M G" uniqKey="Roncarolo M" first="M. G." last="Roncarolo">M. G. Roncarolo</name><affiliation><inist:fA14 i1="02"><s1>San Raffaele Telethon Institute for Gene Therapy</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>6 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Vita-Salute San Raffaele University</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Battaglia, M" sort="Battaglia, M" uniqKey="Battaglia M" first="M." last="Battaglia">M. Battaglia</name><affiliation><inist:fA14 i1="01"><s1>San Raffaele Scientific Institute, Diabetes Research Institute</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">American journal of transplantation : (Print)</title><title level="j" type="abbreviated">Am. j. transplant. : (Print)</title><idno type="ISSN">1600-6135</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">American journal of transplantation : (Print)</title><title level="j" type="abbreviated">Am. j. transplant. : (Print)</title><idno type="ISSN">1600-6135</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Graft</term><term>Immune tolerance</term><term>Langerhans islet</term><term>Spleen</term><term>Surgery</term><term>T regulatory cell</term><term>Transplantation</term><term>Treatment</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Greffe</term><term>Tolérance immune</term><term>Transplantation</term><term>Traitement</term><term>Ilot Langerhans</term><term>Rate</term><term>Chirurgie</term><term>Lymphocyte T régulateur</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The immune system is comprised of several CD4<sup>+</sup> T regulatory (Treg) cell types, of which two, the Foxp3<sup>+</sup> Treg and T regulatory type 1 (Tr1) cells, have frequently been associated with transplant tolerance. However, whether and how these two Treg-cell types synergize to promote allograft tolerance remains unknown. We previously developed a mouse model of allogeneic transplantation in which a specific immunomodulatory treatment leads to transplant tolerance through both Foxp3<sup>+</sup> Treg and Tr1 cells. Here, we show that Foxp3<sup>+</sup> Treg cells exert their regulatory function within the allograft and initiate engraftment locally and in a non-antigen (Ag) specific manner. Whereas CD4<sup>+</sup>CD25<sup>-</sup> T cells, which contain Tr1 cells, act from the spleen and are key to the maintenance of long-term tolerance. Importantly, the role of Foxp3<sup>+</sup> Treg and Tr1 cells is not redundant once they are simultaneously expanded/induced in the same host. Moreover, our data show that long-term tolerance induced by Foxp3<sup>+</sup> Treg-cell transfer is sustained by splenic Tr1 cells and functionally moves from the allograft to the spleen.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>1600-6135</s0></fA01><fA03 i2="1"><s0>Am. j. transplant. : (Print)</s0></fA03><fA05><s2>13</s2></fA05><fA06><s2>8</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Transplant Tolerance to Pancreatic Islets Is Initiated in the Graft and Sustained in the Spleen</s1></fA08><fA11 i1="01" i2="1"><s1>GAGLIANI (N.)</s1></fA11><fA11 i1="02" i2="1"><s1>JOFRA (T.)</s1></fA11><fA11 i1="03" i2="1"><s1>VALLE (A.)</s1></fA11><fA11 i1="04" i2="1"><s1>STABILINI (A.)</s1></fA11><fA11 i1="05" i2="1"><s1>MORSIANI (C.)</s1></fA11><fA11 i1="06" i2="1"><s1>GREGORI (S.)</s1></fA11><fA11 i1="07" i2="1"><s1>DENG (S.)</s1></fA11><fA11 i1="08" i2="1"><s1>ROTHSTEIN (D. M.)</s1></fA11><fA11 i1="09" i2="1"><s1>ATKINSON (M.)</s1></fA11><fA11 i1="10" i2="1"><s1>KAMANAKA (M.)</s1></fA11><fA11 i1="11" i2="1"><s1>FLAVELL (R. A.)</s1></fA11><fA11 i1="12" i2="1"><s1>RONCAROLO (M. G.)</s1></fA11><fA11 i1="13" i2="1"><s1>BATTAGLIA (M.)</s1></fA11><fA14 i1="01"><s1>San Raffaele Scientific Institute, Diabetes Research Institute</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>13 aut.</sZ></fA14><fA14 i1="02"><s1>San Raffaele Telethon Institute for Gene Therapy</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>6 aut.</sZ><sZ>12 aut.</sZ></fA14><fA14 i1="03"><s1>Vita-Salute San Raffaele University</s1><s2>Milan</s2><s3>ITA</s3><sZ>1 aut.</sZ><sZ>12 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Medicine, Yale University School of Medicine</s1><s2>New Haven, CT</s2><s3>USA</s3><sZ>7 aut.</sZ></fA14><fA14 i1="05"><s1>Starzl Transplantation Institute, University of Pittsburgh Medical Center</s1><s2>Pittsburgh, PA</s2><s3>USA</s3><sZ>8 aut.</sZ></fA14><fA14 i1="06"><s1>Department of Pathology, The University of Florida</s1><s2>Gainesville, FL</s2><s3>USA</s3><sZ>9 aut.</sZ></fA14><fA14 i1="07"><s1>Department of Immunobiology, Yale University School of Medicine</s1><s2>New Haven, CT</s2><s3>USA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></fA14><fA14 i1="08"><s1>Howard Hughes Medical Institute</s1><s2>New Haven, CT</s2><s3>USA</s3><sZ>11 aut.</sZ></fA14><fA20><s1>1963-1975</s1></fA20><fA21><s1>2013</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>27587</s2><s5>354000501930860060</s5></fA43><fA44><s0>0000</s0><s1>© 2013 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>33 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>13-0285793</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>American journal of transplantation : (Print)</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>The immune system is comprised of several CD4<sup>+</sup> T regulatory (Treg) cell types, of which two, the Foxp3<sup>+</sup> Treg and T regulatory type 1 (Tr1) cells, have frequently been associated with transplant tolerance. However, whether and how these two Treg-cell types synergize to promote allograft tolerance remains unknown. We previously developed a mouse model of allogeneic transplantation in which a specific immunomodulatory treatment leads to transplant tolerance through both Foxp3<sup>+</sup> Treg and Tr1 cells. Here, we show that Foxp3<sup>+</sup> Treg cells exert their regulatory function within the allograft and initiate engraftment locally and in a non-antigen (Ag) specific manner. Whereas CD4<sup>+</sup>CD25<sup>-</sup> T cells, which contain Tr1 cells, act from the spleen and are key to the maintenance of long-term tolerance. Importantly, the role of Foxp3<sup>+</sup> Treg and Tr1 cells is not redundant once they are simultaneously expanded/induced in the same host. Moreover, our data show that long-term tolerance induced by Foxp3<sup>+</sup> Treg-cell transfer is sustained by splenic Tr1 cells and functionally moves from the allograft to the spleen.</s0></fC01><fC02 i1="01" i2="X"><s0>002B25</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Greffe</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Graft</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Injerto</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Tolérance immune</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Immune tolerance</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Tolerancia inmune</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Transplantation</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Transplantation</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Trasplantación</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Traitement</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Treatment</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Tratamiento</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Ilot Langerhans</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Langerhans islet</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Isla Langerhans</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Rate</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Spleen</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Bazo</s0><s5>06</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Chirurgie</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Surgery</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Cirugía</s0><s5>07</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Lymphocyte T régulateur</s0><s4>CD</s4><s5>96</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>T regulatory cell</s0><s4>CD</s4><s5>96</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Lifocito T regulador</s0><s4>CD</s4><s5>96</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Pancréas endocrine</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Endocrine pancreas</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Páncreas endocrino</s0><s5>37</s5></fC07><fN21><s1>273</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 13-0285793 INIST</NO><ET>Transplant Tolerance to Pancreatic Islets Is Initiated in the Graft and Sustained in the Spleen</ET><AU>GAGLIANI (N.); JOFRA (T.); VALLE (A.); STABILINI (A.); MORSIANI (C.); GREGORI (S.); DENG (S.); ROTHSTEIN (D. M.); ATKINSON (M.); KAMANAKA (M.); FLAVELL (R. A.); RONCAROLO (M. G.); BATTAGLIA (M.)</AU><AF>San Raffaele Scientific Institute, Diabetes Research Institute/Milan/Italie (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 13 aut.); San Raffaele Telethon Institute for Gene Therapy/Milan/Italie (1 aut., 6 aut., 12 aut.); Vita-Salute San Raffaele University/Milan/Italie (1 aut., 12 aut.); Department of Medicine, Yale University School of Medicine/New Haven, CT/Etats-Unis (7 aut.); Starzl Transplantation Institute, University of Pittsburgh Medical Center/Pittsburgh, PA/Etats-Unis (8 aut.); Department of Pathology, The University of Florida/Gainesville, FL/Etats-Unis (9 aut.); Department of Immunobiology, Yale University School of Medicine/New Haven, CT/Etats-Unis (10 aut., 11 aut.); Howard Hughes Medical Institute/New Haven, CT/Etats-Unis (11 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>American journal of transplantation : (Print); ISSN 1600-6135; Etats-Unis; Da. 2013; Vol. 13; No. 8; Pp. 1963-1975; Bibl. 33 ref.</SO><LA>Anglais</LA><EA>The immune system is comprised of several CD4<sup>+</sup> T regulatory (Treg) cell types, of which two, the Foxp3<sup>+</sup> Treg and T regulatory type 1 (Tr1) cells, have frequently been associated with transplant tolerance. However, whether and how these two Treg-cell types synergize to promote allograft tolerance remains unknown. We previously developed a mouse model of allogeneic transplantation in which a specific immunomodulatory treatment leads to transplant tolerance through both Foxp3<sup>+</sup> Treg and Tr1 cells. Here, we show that Foxp3<sup>+</sup> Treg cells exert their regulatory function within the allograft and initiate engraftment locally and in a non-antigen (Ag) specific manner. Whereas CD4<sup>+</sup>CD25<sup>-</sup> T cells, which contain Tr1 cells, act from the spleen and are key to the maintenance of long-term tolerance. Importantly, the role of Foxp3<sup>+</sup> Treg and Tr1 cells is not redundant once they are simultaneously expanded/induced in the same host. Moreover, our data show that long-term tolerance induced by Foxp3<sup>+</sup> Treg-cell transfer is sustained by splenic Tr1 cells and functionally moves from the allograft to the spleen.</EA><CC>002B25</CC><FD>Greffe; Tolérance immune; Transplantation; Traitement; Ilot Langerhans; Rate; Chirurgie; Lymphocyte T régulateur</FD><FG>Pancréas endocrine</FG><ED>Graft; Immune tolerance; Transplantation; Treatment; Langerhans islet; Spleen; Surgery; T regulatory cell</ED><EG>Endocrine pancreas</EG><SD>Injerto; Tolerancia inmune; Trasplantación; Tratamiento; Isla Langerhans; Bazo; Cirugía; Lifocito T regulador</SD><LO>INIST-27587.354000501930860060</LO><ID>13-0285793</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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