Adenosine triphosphate-competitive mTOR inhibitors: a new class of immunosuppressive agents that inhibit allograft rejection
Identifieur interne : 004063 ( Main/Exploration ); précédent : 004062; suivant : 004064Adenosine triphosphate-competitive mTOR inhibitors: a new class of immunosuppressive agents that inhibit allograft rejection
Auteurs : B. R. Rosborough [États-Unis] ; D. Raïch-Regué [États-Unis] ; Q. Liu [États-Unis] ; R. Venkataramanan [États-Unis] ; H. R. Turnquist [États-Unis] ; A. W. Thomson [États-Unis]Source :
- American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons [ 1600-6135 ] ; 2014.
Descripteurs français
- KwdFr :
- Adénosine triphosphate (métabolisme), Amorces ADN, Animaux, Fixation compétitive, Immunosuppresseurs (pharmacologie), Lymphocytes T CD4+ (), Lymphocytes T CD4+ (cytologie), Lymphocytes T CD8+ (), Lymphocytes T CD8+ (cytologie), Morpholines (pharmacocinétique), Morpholines (pharmacologie), Mâle, Prolifération cellulaire (), Rejet du greffon (), Réaction de polymérisation en chaîne, Sirolimus (pharmacocinétique), Sirolimus (pharmacologie), Souris, Souris de lignée C57BL, Survie du greffon, Séquence nucléotidique, Sérine-thréonine kinases TOR (métabolisme).
- MESH :
- cytologie : Lymphocytes T CD4+, Lymphocytes T CD8+.
- métabolisme : Adénosine triphosphate, Sérine-thréonine kinases TOR.
- pharmacocinétique : Morpholines, Sirolimus.
- pharmacologie : Immunosuppresseurs, Morpholines, Sirolimus.
- Amorces ADN, Animaux, Fixation compétitive, Lymphocytes T CD4+, Lymphocytes T CD8+, Mâle, Prolifération cellulaire, Rejet du greffon, Réaction de polymérisation en chaîne, Souris, Souris de lignée C57BL, Survie du greffon, Séquence nucléotidique.
English descriptors
- KwdEn :
- Adenosine Triphosphate (metabolism), Animals, Base Sequence, Binding, Competitive, CD4-Positive T-Lymphocytes (cytology), CD4-Positive T-Lymphocytes (drug effects), CD8-Positive T-Lymphocytes (cytology), CD8-Positive T-Lymphocytes (drug effects), Cell Proliferation (drug effects), DNA Primers, Graft Rejection (prevention & control), Graft Survival, Immunosuppressive Agents (pharmacology), Male, Mice, Mice, Inbred C57BL, Morpholines (pharmacokinetics), Morpholines (pharmacology), Polymerase Chain Reaction, Sirolimus (pharmacokinetics), Sirolimus (pharmacology), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , metabolism : Adenosine Triphosphate, TOR Serine-Threonine Kinases.
- cytology : CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes.
- drug effects : CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Cell Proliferation.
- chemical , pharmacokinetics : Morpholines, Sirolimus.
- chemical , pharmacology : Immunosuppressive Agents, Morpholines, Sirolimus.
- prevention & control : Graft Rejection.
- Animals, Base Sequence, Binding, Competitive, DNA Primers, Graft Survival, Male, Mice, Mice, Inbred C57BL, Polymerase Chain Reaction.
Abstract
The mechanistic/mammalian target of rapamycin (mTOR) is inhibited clinically to suppress T cell function and prevent allograft rejection. mTOR is the kinase subunit of two mTOR-containing complexes, mTOR complex (mTORC) 1 and 2. Although mTORC1 is inhibited by the macrolide immunosuppressant rapamycin (RAPA), its efficacy may be limited by its inability to block mTORC1 completely and its limited effect on mTORC2. Adenosine triphosphate (ATP)-competitive mTOR inhibitors are an emerging class of mTOR inhibitors that compete with ATP at the mTOR active site and inhibit any mTOR-containing complex. Since this class of compounds has not been investigated for their immunosuppressive potential, our goal was to determine the influence of a prototypic ATP-competitive mTOR inhibitor on allograft survival. AZD8055 proved to be a potent suppressor of T cell proliferation. Moreover, a short, 10-day course of the agent successfully prolonged murine MHC-mismatched, vascularized heart transplant survival. This therapeutic effect was associated with increased graft-infiltrating regulatory T cells and reduced CD4+ and CD8+ T cell IFN-γ production. These studies establish for the first time, that ATP-competitive mTOR inhibition can prolong organ allograft survival and warrant further investigation of this next generation mTOR inhibitors.
Url:
DOI: 10.1111/ajt.12799
PubMed: 25307040
PubMed Central: 4196715
Affiliations:
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Le document en format XML
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(metabolism)</term><term>Animals</term><term>Base Sequence</term><term>Binding, Competitive</term><term>CD4-Positive T-Lymphocytes (cytology)</term><term>CD4-Positive T-Lymphocytes (drug effects)</term><term>CD8-Positive T-Lymphocytes (cytology)</term><term>CD8-Positive T-Lymphocytes (drug effects)</term><term>Cell Proliferation (drug effects)</term><term>DNA Primers</term><term>Graft Rejection (prevention & control)</term><term>Graft Survival</term><term>Immunosuppressive Agents (pharmacology)</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Morpholines (pharmacokinetics)</term><term>Morpholines (pharmacology)</term><term>Polymerase Chain Reaction</term><term>Sirolimus (pharmacokinetics)</term><term>Sirolimus (pharmacology)</term><term>TOR Serine-Threonine Kinases (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adénosine triphosphate (métabolisme)</term><term>Amorces ADN</term><term>Animaux</term><term>Fixation compétitive</term><term>Immunosuppresseurs (pharmacologie)</term><term>Lymphocytes T CD4+ ()</term><term>Lymphocytes T CD4+ (cytologie)</term><term>Lymphocytes T CD8+ ()</term><term>Lymphocytes T CD8+ (cytologie)</term><term>Morpholines (pharmacocinétique)</term><term>Morpholines (pharmacologie)</term><term>Mâle</term><term>Prolifération cellulaire ()</term><term>Rejet du greffon ()</term><term>Réaction de polymérisation en chaîne</term><term>Sirolimus (pharmacocinétique)</term><term>Sirolimus (pharmacologie)</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Survie du greffon</term><term>Séquence nucléotidique</term><term>Sérine-thréonine kinases TOR (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adenosine Triphosphate</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Lymphocytes T CD4+</term><term>Lymphocytes T 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type="abstract" xml:lang="en"><p id="P1">The mechanistic/mammalian target of rapamycin (mTOR) is inhibited clinically to suppress T cell function and prevent allograft rejection. mTOR is the kinase subunit of two mTOR-containing complexes, mTOR complex (mTORC) 1 and 2. Although mTORC1 is inhibited by the macrolide immunosuppressant rapamycin (RAPA), its efficacy may be limited by its inability to block mTORC1 completely and its limited effect on mTORC2. Adenosine triphosphate (ATP)-competitive mTOR inhibitors are an emerging class of mTOR inhibitors that compete with ATP at the mTOR active site and inhibit any mTOR-containing complex. Since this class of compounds has not been investigated for their immunosuppressive potential, our goal was to determine the influence of a prototypic ATP-competitive mTOR inhibitor on allograft survival. AZD8055 proved to be a potent suppressor of T cell proliferation. Moreover, a short, 10-day course of the agent successfully prolonged murine MHC-mismatched, vascularized heart transplant survival. This therapeutic effect was associated with increased graft-infiltrating regulatory T cells and reduced CD4<sup>+</sup> and CD8<sup>+</sup> T cell IFN-γ production. These studies establish for the first time, that ATP-competitive mTOR inhibition can prolong organ allograft survival and warrant further investigation of this next generation mTOR inhibitors.</p></div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Pennsylvanie</li></region></list><tree><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Rosborough, B R" sort="Rosborough, B R" uniqKey="Rosborough B" first="B. R." last="Rosborough">B. R. Rosborough</name></region><name sortKey="Liu, Q" sort="Liu, Q" uniqKey="Liu Q" first="Q." last="Liu">Q. Liu</name><name sortKey="Raich Regue, D" sort="Raich Regue, D" uniqKey="Raich Regue D" first="D." last="Raïch-Regué">D. Raïch-Regué</name><name sortKey="Thomson, A W" sort="Thomson, A W" uniqKey="Thomson A" first="A. W." last="Thomson">A. W. Thomson</name><name sortKey="Thomson, A W" sort="Thomson, A W" uniqKey="Thomson A" first="A. W." last="Thomson">A. W. Thomson</name><name sortKey="Turnquist, H R" sort="Turnquist, H R" uniqKey="Turnquist H" first="H. R." last="Turnquist">H. R. Turnquist</name><name sortKey="Turnquist, H R" sort="Turnquist, H R" uniqKey="Turnquist H" first="H. R." last="Turnquist">H. R. Turnquist</name><name sortKey="Venkataramanan, R" sort="Venkataramanan, R" uniqKey="Venkataramanan R" first="R." last="Venkataramanan">R. Venkataramanan</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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