Too much of a good thing? Tim-3 and TCR signaling in T cell exhaustion.
Identifieur interne : 000B46 ( Main/Exploration ); précédent : 000B45; suivant : 000B47Too much of a good thing? Tim-3 and TCR signaling in T cell exhaustion.
Auteurs : Robert L. Ferris [États-Unis] ; Binfeng Lu [États-Unis] ; Lawrence P. Kane [États-Unis]Source :
- Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2014.
Descripteurs français
- KwdFr :
- Activation des lymphocytes (immunologie), Animaux, Antigènes CD (biosynthèse), Antigènes CD (immunologie), Cytokines (biosynthèse), Hepacivirus (immunologie), Humains, Lymphocytes T CD4+ (immunologie), Lymphocytes T CD8+ (immunologie), Microenvironnement tumoral (immunologie), Prolifération cellulaire, Protéines de répression (biosynthèse), Protéines membranaires (biosynthèse), Protéines membranaires (immunologie), Récepteur cellulaire-2 du virus de l'hépatite A, Récepteur-1 de mort cellulaire programmée (biosynthèse), Récepteur-1 de mort cellulaire programmée (immunologie), Récepteurs aux antigènes des cellules T (génétique), Récepteurs aux antigènes des cellules T (immunologie), Souris, Transduction du signal (immunologie), VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (immunologie).
- MESH :
- biosynthèse : Antigènes CD, Cytokines, Protéines de répression, Protéines membranaires, Récepteur-1 de mort cellulaire programmée.
- génétique : Récepteurs aux antigènes des cellules T.
- immunologie : Activation des lymphocytes, Antigènes CD, Hepacivirus, Lymphocytes T CD4+, Lymphocytes T CD8+, Microenvironnement tumoral, Protéines membranaires, Récepteur-1 de mort cellulaire programmée, Récepteurs aux antigènes des cellules T, Transduction du signal, VIH-1 (Virus de l'Immunodéficience Humaine de type 1).
- Animaux, Humains, Prolifération cellulaire, Récepteur cellulaire-2 du virus de l'hépatite A, Souris.
English descriptors
- KwdEn :
- Animals, Antigens, CD (biosynthesis), Antigens, CD (immunology), CD4-Positive T-Lymphocytes (immunology), CD8-Positive T-Lymphocytes (immunology), Cell Proliferation, Cytokines (biosynthesis), HIV-1 (immunology), Hepacivirus (immunology), Hepatitis A Virus Cellular Receptor 2, Humans, Lymphocyte Activation (immunology), Membrane Proteins (biosynthesis), Membrane Proteins (immunology), Mice, Programmed Cell Death 1 Receptor (biosynthesis), Programmed Cell Death 1 Receptor (immunology), Receptors, Antigen, T-Cell (genetics), Receptors, Antigen, T-Cell (immunology), Repressor Proteins (biosynthesis), Signal Transduction (immunology), Tumor Microenvironment (immunology).
- MESH :
- chemical , biosynthesis : Antigens, CD, Cytokines, Membrane Proteins, Programmed Cell Death 1 Receptor, Repressor Proteins.
- chemical , genetics : Receptors, Antigen, T-Cell.
- chemical , immunology : Antigens, CD, Membrane Proteins, Programmed Cell Death 1 Receptor, Receptors, Antigen, T-Cell.
- immunology : CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, HIV-1, Hepacivirus, Lymphocyte Activation, Signal Transduction, Tumor Microenvironment.
- Animals, Cell Proliferation, Hepatitis A Virus Cellular Receptor 2, Humans, Mice.
Abstract
T cell exhaustion is thought to be a natural mechanism for limiting immune pathology, although it may be desirable to circumvent this mechanism to help eliminate viral reservoirs or tumors. Although there are no definitive markers, a fingerprint for exhausted T cells has been described that includes the transmembrane proteins PD-1, LAG3, and Tim-3. However, apart from the recruitment of tyrosine phosphatases to PD-1, little is known about the biochemical mechanisms by which these proteins contribute to the development or maintenance of exhaustion. Tim-3 contains no known motifs for the recruitment of inhibitory phosphatases, but it may actually increase signaling downstream of TCR/CD3, at least under acute conditions. Other studies showed that T cell exhaustion results from chronic stimulation that extends the effector phase of T cell activation, at the expense of T cell memory. We suggest that Tim-3 may contribute to T cell exhaustion by enhancing TCR-signaling pathways.
DOI: 10.4049/jimmunol.1400557
PubMed: 25086175
Affiliations:
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Le document en format XML
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Tim-3 and TCR signaling in T cell exhaustion.</title><author><name sortKey="Ferris, Robert L" sort="Ferris, Robert L" uniqKey="Ferris R" first="Robert L" last="Ferris">Robert L. 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type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antigens, CD (biosynthesis)</term><term>Antigens, CD (immunology)</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>CD8-Positive T-Lymphocytes (immunology)</term><term>Cell Proliferation</term><term>Cytokines (biosynthesis)</term><term>HIV-1 (immunology)</term><term>Hepacivirus (immunology)</term><term>Hepatitis A Virus Cellular Receptor 2</term><term>Humans</term><term>Lymphocyte Activation (immunology)</term><term>Membrane Proteins (biosynthesis)</term><term>Membrane Proteins (immunology)</term><term>Mice</term><term>Programmed Cell Death 1 Receptor (biosynthesis)</term><term>Programmed Cell Death 1 Receptor (immunology)</term><term>Receptors, Antigen, T-Cell (genetics)</term><term>Receptors, Antigen, T-Cell (immunology)</term><term>Repressor Proteins (biosynthesis)</term><term>Signal Transduction (immunology)</term><term>Tumor Microenvironment (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation des lymphocytes (immunologie)</term><term>Animaux</term><term>Antigènes CD (biosynthèse)</term><term>Antigènes CD (immunologie)</term><term>Cytokines (biosynthèse)</term><term>Hepacivirus (immunologie)</term><term>Humains</term><term>Lymphocytes T CD4+ (immunologie)</term><term>Lymphocytes T CD8+ (immunologie)</term><term>Microenvironnement tumoral (immunologie)</term><term>Prolifération cellulaire</term><term>Protéines de répression (biosynthèse)</term><term>Protéines membranaires (biosynthèse)</term><term>Protéines membranaires (immunologie)</term><term>Récepteur cellulaire-2 du virus de l'hépatite A</term><term>Récepteur-1 de mort cellulaire programmée (biosynthèse)</term><term>Récepteur-1 de mort cellulaire programmée (immunologie)</term><term>Récepteurs aux antigènes des cellules T (génétique)</term><term>Récepteurs aux antigènes des cellules T (immunologie)</term><term>Souris</term><term>Transduction du signal (immunologie)</term><term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1) (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Antigens, CD</term><term>Cytokines</term><term>Membrane Proteins</term><term>Programmed Cell Death 1 Receptor</term><term>Repressor Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, Antigen, T-Cell</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antigens, CD</term><term>Membrane Proteins</term><term>Programmed Cell Death 1 Receptor</term><term>Receptors, Antigen, T-Cell</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Antigènes CD</term><term>Cytokines</term><term>Protéines de répression</term><term>Protéines membranaires</term><term>Récepteur-1 de mort cellulaire programmée</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Récepteurs aux antigènes des cellules T</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Activation des lymphocytes</term><term>Antigènes CD</term><term>Hepacivirus</term><term>Lymphocytes T CD4+</term><term>Lymphocytes T CD8+</term><term>Microenvironnement tumoral</term><term>Protéines membranaires</term><term>Récepteur-1 de mort cellulaire programmée</term><term>Récepteurs aux antigènes des cellules T</term><term>Transduction du signal</term><term>VIH-1 (Virus de l'Immunodéficience Humaine de type 1)</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term><term>CD8-Positive T-Lymphocytes</term><term>HIV-1</term><term>Hepacivirus</term><term>Lymphocyte Activation</term><term>Signal Transduction</term><term>Tumor Microenvironment</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Proliferation</term><term>Hepatitis A Virus Cellular Receptor 2</term><term>Humans</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Prolifération cellulaire</term><term>Récepteur cellulaire-2 du virus de l'hépatite A</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">T cell exhaustion is thought to be a natural mechanism for limiting immune pathology, although it may be desirable to circumvent this mechanism to help eliminate viral reservoirs or tumors. Although there are no definitive markers, a fingerprint for exhausted T cells has been described that includes the transmembrane proteins PD-1, LAG3, and Tim-3. However, apart from the recruitment of tyrosine phosphatases to PD-1, little is known about the biochemical mechanisms by which these proteins contribute to the development or maintenance of exhaustion. Tim-3 contains no known motifs for the recruitment of inhibitory phosphatases, but it may actually increase signaling downstream of TCR/CD3, at least under acute conditions. Other studies showed that T cell exhaustion results from chronic stimulation that extends the effector phase of T cell activation, at the expense of T cell memory. We suggest that Tim-3 may contribute to T cell exhaustion by enhancing TCR-signaling pathways.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Pennsylvanie</li></region><settlement><li>Pittsburgh</li></settlement></list><tree><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Ferris, Robert L" sort="Ferris, Robert L" uniqKey="Ferris R" first="Robert L" last="Ferris">Robert L. Ferris</name></region><name sortKey="Kane, Lawrence P" sort="Kane, Lawrence P" uniqKey="Kane L" first="Lawrence P" last="Kane">Lawrence P. Kane</name><name sortKey="Lu, Binfeng" sort="Lu, Binfeng" uniqKey="Lu B" first="Binfeng" last="Lu">Binfeng Lu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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