mTOR limits the recruitment of CD11b+Gr1+Ly6Chigh myeloid-derived suppressor cells in protecting against murine immunological hepatic injury.
Identifieur interne : 000E90 ( Main/Corpus ); précédent : 000E89; suivant : 000E91mTOR limits the recruitment of CD11b+Gr1+Ly6Chigh myeloid-derived suppressor cells in protecting against murine immunological hepatic injury.
Auteurs : Yan Zhang ; Yujing Bi ; Hui Yang ; Xi Chen ; Huanrong Liu ; Yun Lu ; Zhengguo Zhang ; Jiongbo Liao ; Shan Yang ; Yiwei Chu ; Ruifu Yang ; Guangwei LiuSource :
- Journal of leukocyte biology [ 1938-3673 ] ; 2014.
English descriptors
- KwdEn :
- Animals (MeSH), Antigens, Ly (analysis), CD11b Antigen (analysis), Cell Movement (drug effects), Immune Tolerance (MeSH), Liver Diseases (immunology), Mice (MeSH), Myeloid Cells (immunology), Myeloid Cells (physiology), Nitric Oxide (biosynthesis), Receptors, Chemokine (analysis), Signal Transduction (physiology), Sirolimus (pharmacology), TOR Serine-Threonine Kinases (physiology).
- MESH :
- chemical , analysis : Antigens, Ly, CD11b Antigen, Receptors, Chemokine.
- chemical , biosynthesis : Nitric Oxide.
- drug effects : Cell Movement.
- immunology : Liver Diseases, Myeloid Cells.
- chemical , pharmacology : Sirolimus.
- physiology : Myeloid Cells, Signal Transduction, TOR Serine-Threonine Kinases.
- Animals, Immune Tolerance, Mice.
Abstract
The mTOR pathway integrates diverse environmental inputs, including immune signals and metabolic cues, to direct the innate and adaptive immune responses. MDSCs are a heterogeneous cell population that plays a crucial regulatory effect in immune-related diseases. However, whether mTOR signaling affects the functions of MDSCs remains largely unknown. Here, we show that mTOR signaling is a pivotal negative determinant of MDSC recruitment in IMH disease. In the context of IMH, inhibition of mTOR with rapamycin in CD11b⁺Gr1⁺ MDSCs mediates protection against IMH and serves as a functional, suppressive immune modulator that results in increased CD11b⁺Gr1⁺Ly6C(high) MDSC recruitment to inflammatory sites. In agreement with this, mTOR down-regulation promotes CD11b⁺Gr1⁺Ly6C(high) MDSC migration in vitro and in vivo. Mechanistically, mTOR activity down-regulation in MDSCs induced iNOS expression and NO production. Pharmacologic inhibition of iNOS completely eliminated MDSC recruitment. This study identifies MDSCs as an essential component for protection against IMH following rapamycin treatment. Rapamycin treatment or mTOR inhibition promotes CD11b⁺Gr1⁺Ly6C(high) MDSC recruitment and is critically required for protection against hepatic injury. This study further validates the targeting of mTOR signaling as a potential therapeutic approach to IMH-related diseases.
DOI: 10.1189/jlb.0913473
PubMed: 24569105
Links to Exploration step
pubmed:24569105Le document en format XML
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<term>Immune Tolerance (MeSH)</term>
<term>Liver Diseases (immunology)</term>
<term>Mice (MeSH)</term>
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<term>Myeloid Cells (physiology)</term>
<term>Nitric Oxide (biosynthesis)</term>
<term>Receptors, Chemokine (analysis)</term>
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<front><div type="abstract" xml:lang="en">The mTOR pathway integrates diverse environmental inputs, including immune signals and metabolic cues, to direct the innate and adaptive immune responses. MDSCs are a heterogeneous cell population that plays a crucial regulatory effect in immune-related diseases. However, whether mTOR signaling affects the functions of MDSCs remains largely unknown. Here, we show that mTOR signaling is a pivotal negative determinant of MDSC recruitment in IMH disease. In the context of IMH, inhibition of mTOR with rapamycin in CD11b⁺Gr1⁺ MDSCs mediates protection against IMH and serves as a functional, suppressive immune modulator that results in increased CD11b⁺Gr1⁺Ly6C(high) MDSC recruitment to inflammatory sites. In agreement with this, mTOR down-regulation promotes CD11b⁺Gr1⁺Ly6C(high) MDSC migration in vitro and in vivo. Mechanistically, mTOR activity down-regulation in MDSCs induced iNOS expression and NO production. Pharmacologic inhibition of iNOS completely eliminated MDSC recruitment. This study identifies MDSCs as an essential component for protection against IMH following rapamycin treatment. Rapamycin treatment or mTOR inhibition promotes CD11b⁺Gr1⁺Ly6C(high) MDSC recruitment and is critically required for protection against hepatic injury. This study further validates the targeting of mTOR signaling as a potential therapeutic approach to IMH-related diseases.</div>
</front>
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<Abstract><AbstractText>The mTOR pathway integrates diverse environmental inputs, including immune signals and metabolic cues, to direct the innate and adaptive immune responses. MDSCs are a heterogeneous cell population that plays a crucial regulatory effect in immune-related diseases. However, whether mTOR signaling affects the functions of MDSCs remains largely unknown. Here, we show that mTOR signaling is a pivotal negative determinant of MDSC recruitment in IMH disease. In the context of IMH, inhibition of mTOR with rapamycin in CD11b⁺Gr1⁺ MDSCs mediates protection against IMH and serves as a functional, suppressive immune modulator that results in increased CD11b⁺Gr1⁺Ly6C(high) MDSC recruitment to inflammatory sites. In agreement with this, mTOR down-regulation promotes CD11b⁺Gr1⁺Ly6C(high) MDSC migration in vitro and in vivo. Mechanistically, mTOR activity down-regulation in MDSCs induced iNOS expression and NO production. Pharmacologic inhibition of iNOS completely eliminated MDSC recruitment. This study identifies MDSCs as an essential component for protection against IMH following rapamycin treatment. Rapamycin treatment or mTOR inhibition promotes CD11b⁺Gr1⁺Ly6C(high) MDSC recruitment and is critically required for protection against hepatic injury. This study further validates the targeting of mTOR signaling as a potential therapeutic approach to IMH-related diseases.</AbstractText>
<CopyrightInformation>© 2014 Society for Leukocyte Biology.</CopyrightInformation>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Yan</ForeName>
<Initials>Y</Initials>
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