Programmed Death-1 Inhibition of Phosphatidylinositol 3-Kinase/AKT/Mechanistic Target of Rapamycin Signaling Impairs Sarcoidosis CD4+ T Cell Proliferation.
Identifieur interne : 000770 ( Main/Exploration ); précédent : 000769; suivant : 000771Programmed Death-1 Inhibition of Phosphatidylinositol 3-Kinase/AKT/Mechanistic Target of Rapamycin Signaling Impairs Sarcoidosis CD4+ T Cell Proliferation.
Auteurs : Lindsay J. Celada [États-Unis] ; Joseph E. Rotsinger ; Anjuli Young ; Guzel Shaginurova [États-Unis] ; Debresha Shelton ; Charlene Hawkins ; Wonder P. Drake [États-Unis]Source :
- American journal of respiratory cell and molecular biology [ 1535-4989 ] ; 2017.
Descripteurs français
- KwdFr :
- Adulte (MeSH), Adulte d'âge moyen (MeSH), Démographie (MeSH), Femelle (MeSH), Humains (MeSH), Jeune adulte (MeSH), Lymphocytes T CD4+ (immunologie), Mâle (MeSH), Phosphatidylinositol 3-kinase (métabolisme), Prolifération cellulaire (MeSH), Protéines proto-oncogènes c-akt (métabolisme), Récepteur-1 de mort cellulaire programmée (métabolisme), Régulation de l'expression des gènes (MeSH), Sarcoïdose (anatomopathologie), Sarcoïdose (immunologie), Sarcoïdose (métabolisme), Sujet âgé (MeSH), Sérine-thréonine kinases TOR (métabolisme), Transduction du signal (MeSH), Études cas-témoins (MeSH).
- MESH :
- anatomopathologie : Sarcoïdose.
- immunologie : Lymphocytes T CD4+, Sarcoïdose.
- métabolisme : Phosphatidylinositol 3-kinase, Protéines proto-oncogènes c-akt, Récepteur-1 de mort cellulaire programmée, Sarcoïdose, Sérine-thréonine kinases TOR.
- Adulte, Adulte d'âge moyen, Démographie, Femelle, Humains, Jeune adulte, Mâle, Prolifération cellulaire, Régulation de l'expression des gènes, Sujet âgé, Transduction du signal, Études cas-témoins.
English descriptors
- KwdEn :
- Adult (MeSH), Aged (MeSH), CD4-Positive T-Lymphocytes (immunology), Case-Control Studies (MeSH), Cell Proliferation (MeSH), Demography (MeSH), Female (MeSH), Gene Expression Regulation (MeSH), Humans (MeSH), Male (MeSH), Middle Aged (MeSH), Phosphatidylinositol 3-Kinase (metabolism), Programmed Cell Death 1 Receptor (metabolism), Proto-Oncogene Proteins c-akt (metabolism), Sarcoidosis (immunology), Sarcoidosis (metabolism), Sarcoidosis (pathology), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (metabolism), Young Adult (MeSH).
- MESH :
- chemical , metabolism : Phosphatidylinositol 3-Kinase, Programmed Cell Death 1 Receptor, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases.
- immunology : CD4-Positive T-Lymphocytes, Sarcoidosis.
- metabolism : Sarcoidosis.
- pathology : Sarcoidosis.
- Adult, Aged, Case-Control Studies, Cell Proliferation, Demography, Female, Gene Expression Regulation, Humans, Male, Middle Aged, Signal Transduction, Young Adult.
Abstract
Patients with progressive sarcoidosis exhibit increased expression of programmed death-1 (PD-1) receptor on their CD4+ T cells. Up-regulation of this marker of T cell exhaustion is associated with a reduction in the proliferative response to T cell receptor (TCR) stimulation, a defect that is reversed by PD-1 pathway blockade. Genome-wide association studies and microarray analyses have correlated signaling downstream from the TCR with sarcoidosis disease severity, but the mechanism is not yet known. Reduced phosphatidylinositol 3-kinase (PI3K)/AKT expression inhibits proliferation by inhibiting cell cycle progression. To test the hypothesis that PD-1 expression attenuates TCR-dependent activation of PI3K/AKT activity in progressive systemic sarcoidosis, we analyzed PI3K/AKT/mechanistic target of rapamycin (mTOR) expression at baseline and after PD-1 pathway blockade in CD4+ T cells isolated from patients with sarcoidosis and healthy control subjects. We confirmed an increased percentage of PD-1+ CD4+ T cells and reduced proliferative capacity in patients with sarcoidosis compared with healthy control subjects (P < 0.001). There was a negative correlation with PD-1 expression and proliferative capacity (r = -0.70, P < 0.001). Expression of key mediators of cell cycle progression, including PI3K and AKT, were significantly decreased. Gene and protein expression levels reverted to healthy control levels after PD-1 pathway blockade. Reduction in sarcoidosis CD4+ T cell proliferative capacity is secondary to altered expression of key mediators of cell cycle progression, including the PI3K/AKT/mTOR pathway, via PD-1 up-regulation. This supports the concept that PD-1 up-regulation drives the immunologic deficits associated with sarcoidosis severity by inducing signaling aberrancies in key mediators of cell cycle progression.
DOI: 10.1165/rcmb.2016-0037OC
PubMed: 27564547
PubMed Central: PMC5248958
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Rotsinger</name><affiliation><nlm:affiliation>1 Division of Infectious Diseases, Department of Medicine, and.</nlm:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Young, Anjuli" sort="Young, Anjuli" uniqKey="Young A" first="Anjuli" last="Young">Anjuli Young</name><affiliation><nlm:affiliation>1 Division of Infectious Diseases, Department of Medicine, and.</nlm:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Shaginurova, Guzel" sort="Shaginurova, Guzel" uniqKey="Shaginurova G" first="Guzel" last="Shaginurova">Guzel Shaginurova</name><affiliation wicri:level="2"><nlm:affiliation>2 Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>2 Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville</wicri:cityArea></affiliation></author><author><name sortKey="Shelton, Debresha" sort="Shelton, Debresha" uniqKey="Shelton D" first="Debresha" last="Shelton">Debresha Shelton</name><affiliation><nlm:affiliation>1 Division of Infectious Diseases, Department of Medicine, and.</nlm:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Hawkins, Charlene" sort="Hawkins, Charlene" uniqKey="Hawkins C" first="Charlene" last="Hawkins">Charlene Hawkins</name><affiliation><nlm:affiliation>1 Division of Infectious Diseases, Department of Medicine, and.</nlm:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Drake, Wonder P" sort="Drake, Wonder P" uniqKey="Drake W" first="Wonder P" last="Drake">Wonder P. Drake</name><affiliation><nlm:affiliation>1 Division of Infectious Diseases, Department of Medicine, and.</nlm:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation><affiliation wicri:level="2"><nlm:affiliation>2 Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>2 Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville</wicri:cityArea></affiliation></author></analytic><series><title level="j">American journal of respiratory cell and molecular biology</title><idno type="eISSN">1535-4989</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult (MeSH)</term><term>Aged (MeSH)</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>Case-Control Studies (MeSH)</term><term>Cell Proliferation (MeSH)</term><term>Demography (MeSH)</term><term>Female (MeSH)</term><term>Gene Expression Regulation (MeSH)</term><term>Humans (MeSH)</term><term>Male (MeSH)</term><term>Middle Aged (MeSH)</term><term>Phosphatidylinositol 3-Kinase (metabolism)</term><term>Programmed Cell Death 1 Receptor (metabolism)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Sarcoidosis (immunology)</term><term>Sarcoidosis (metabolism)</term><term>Sarcoidosis (pathology)</term><term>Signal Transduction (MeSH)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Young Adult (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte (MeSH)</term><term>Adulte d'âge moyen (MeSH)</term><term>Démographie (MeSH)</term><term>Femelle (MeSH)</term><term>Humains (MeSH)</term><term>Jeune adulte (MeSH)</term><term>Lymphocytes T CD4+ (immunologie)</term><term>Mâle (MeSH)</term><term>Phosphatidylinositol 3-kinase (métabolisme)</term><term>Prolifération cellulaire (MeSH)</term><term>Protéines proto-oncogènes c-akt (métabolisme)</term><term>Récepteur-1 de mort cellulaire programmée (métabolisme)</term><term>Régulation de l'expression des gènes (MeSH)</term><term>Sarcoïdose (anatomopathologie)</term><term>Sarcoïdose (immunologie)</term><term>Sarcoïdose (métabolisme)</term><term>Sujet âgé (MeSH)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Transduction du signal (MeSH)</term><term>Études cas-témoins (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Phosphatidylinositol 3-Kinase</term><term>Programmed Cell Death 1 Receptor</term><term>Proto-Oncogene Proteins c-akt</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Sarcoïdose</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Lymphocytes T CD4+</term><term>Sarcoïdose</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term><term>Sarcoidosis</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Sarcoidosis</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Phosphatidylinositol 3-kinase</term><term>Protéines proto-oncogènes c-akt</term><term>Récepteur-1 de mort cellulaire programmée</term><term>Sarcoïdose</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Sarcoidosis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Case-Control Studies</term><term>Cell Proliferation</term><term>Demography</term><term>Female</term><term>Gene Expression Regulation</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Signal Transduction</term><term>Young Adult</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Adulte d'âge moyen</term><term>Démographie</term><term>Femelle</term><term>Humains</term><term>Jeune adulte</term><term>Mâle</term><term>Prolifération cellulaire</term><term>Régulation de l'expression des gènes</term><term>Sujet âgé</term><term>Transduction du signal</term><term>Études cas-témoins</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Patients with progressive sarcoidosis exhibit increased expression of programmed death-1 (PD-1) receptor on their CD4<sup>+</sup> T cells. Up-regulation of this marker of T cell exhaustion is associated with a reduction in the proliferative response to T cell receptor (TCR) stimulation, a defect that is reversed by PD-1 pathway blockade. Genome-wide association studies and microarray analyses have correlated signaling downstream from the TCR with sarcoidosis disease severity, but the mechanism is not yet known. Reduced phosphatidylinositol 3-kinase (PI3K)/AKT expression inhibits proliferation by inhibiting cell cycle progression. To test the hypothesis that PD-1 expression attenuates TCR-dependent activation of PI3K/AKT activity in progressive systemic sarcoidosis, we analyzed PI3K/AKT/mechanistic target of rapamycin (mTOR) expression at baseline and after PD-1 pathway blockade in CD4<sup>+</sup> T cells isolated from patients with sarcoidosis and healthy control subjects. We confirmed an increased percentage of PD-1<sup>+</sup> CD4<sup>+</sup> T cells and reduced proliferative capacity in patients with sarcoidosis compared with healthy control subjects (P < 0.001). There was a negative correlation with PD-1 expression and proliferative capacity (r = -0.70, P < 0.001). Expression of key mediators of cell cycle progression, including PI3K and AKT, were significantly decreased. Gene and protein expression levels reverted to healthy control levels after PD-1 pathway blockade. Reduction in sarcoidosis CD4<sup>+</sup> T cell proliferative capacity is secondary to altered expression of key mediators of cell cycle progression, including the PI3K/AKT/mTOR pathway, via PD-1 up-regulation. This supports the concept that PD-1 up-regulation drives the immunologic deficits associated with sarcoidosis severity by inducing signaling aberrancies in key mediators of cell cycle progression.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27564547</PMID><DateCompleted><Year>2017</Year><Month>06</Month><Day>30</Day></DateCompleted><DateRevised><Year>2019</Year><Month>03</Month><Day>05</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1535-4989</ISSN><JournalIssue CitedMedium="Internet"><Volume>56</Volume><Issue>1</Issue><PubDate><Year>2017</Year><Month>01</Month></PubDate></JournalIssue><Title>American journal of respiratory cell and molecular biology</Title><ISOAbbreviation>Am J Respir Cell Mol Biol</ISOAbbreviation></Journal><ArticleTitle>Programmed Death-1 Inhibition of Phosphatidylinositol 3-Kinase/AKT/Mechanistic Target of Rapamycin Signaling Impairs Sarcoidosis CD4<sup>+</sup> T Cell Proliferation.</ArticleTitle><Pagination><MedlinePgn>74-82</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1165/rcmb.2016-0037OC</ELocationID><Abstract><AbstractText>Patients with progressive sarcoidosis exhibit increased expression of programmed death-1 (PD-1) receptor on their CD4<sup>+</sup> T cells. Up-regulation of this marker of T cell exhaustion is associated with a reduction in the proliferative response to T cell receptor (TCR) stimulation, a defect that is reversed by PD-1 pathway blockade. Genome-wide association studies and microarray analyses have correlated signaling downstream from the TCR with sarcoidosis disease severity, but the mechanism is not yet known. Reduced phosphatidylinositol 3-kinase (PI3K)/AKT expression inhibits proliferation by inhibiting cell cycle progression. To test the hypothesis that PD-1 expression attenuates TCR-dependent activation of PI3K/AKT activity in progressive systemic sarcoidosis, we analyzed PI3K/AKT/mechanistic target of rapamycin (mTOR) expression at baseline and after PD-1 pathway blockade in CD4<sup>+</sup> T cells isolated from patients with sarcoidosis and healthy control subjects. We confirmed an increased percentage of PD-1<sup>+</sup> CD4<sup>+</sup> T cells and reduced proliferative capacity in patients with sarcoidosis compared with healthy control subjects (P < 0.001). There was a negative correlation with PD-1 expression and proliferative capacity (r = -0.70, P < 0.001). Expression of key mediators of cell cycle progression, including PI3K and AKT, were significantly decreased. Gene and protein expression levels reverted to healthy control levels after PD-1 pathway blockade. Reduction in sarcoidosis CD4<sup>+</sup> T cell proliferative capacity is secondary to altered expression of key mediators of cell cycle progression, including the PI3K/AKT/mTOR pathway, via PD-1 up-regulation. This supports the concept that PD-1 up-regulation drives the immunologic deficits associated with sarcoidosis severity by inducing signaling aberrancies in key mediators of cell cycle progression.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Celada</LastName><ForeName>Lindsay J</ForeName><Initials>LJ</Initials><AffiliationInfo><Affiliation>1 Division of Infectious Diseases, Department of Medicine, and.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>2 Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rotsinger</LastName><ForeName>Joseph E</ForeName><Initials>JE</Initials><AffiliationInfo><Affiliation>1 Division of Infectious Diseases, Department of Medicine, and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Young</LastName><ForeName>Anjuli</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>1 Division of Infectious Diseases, Department of Medicine, and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shaginurova</LastName><ForeName>Guzel</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>2 Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shelton</LastName><ForeName>Debresha</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>1 Division of Infectious Diseases, Department of Medicine, and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hawkins</LastName><ForeName>Charlene</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>1 Division of Infectious Diseases, Department of Medicine, and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Drake</LastName><ForeName>Wonder P</ForeName><Initials>WP</Initials><AffiliationInfo><Affiliation>1 Division of Infectious Diseases, Department of Medicine, and.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>2 Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>U01 HL112694</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 DK058404</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL117074</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K24 HL127301</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 HL094296</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 HL069765</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 CA068485</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL083839</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1 RR024975</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Respir Cell Mol Biol</MedlineTA><NlmUniqueID>8917225</NlmUniqueID><ISSNLinking>1044-1549</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C105992">PDCD1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D061026">Programmed Cell Death 1 Receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.137</RegistryNumber><NameOfSubstance UI="D058539">Phosphatidylinositol 3-Kinase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015496" MajorTopicYN="N">CD4-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003710" MajorTopicYN="N">Demography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058539" MajorTopicYN="N">Phosphatidylinositol 3-Kinase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061026" MajorTopicYN="N">Programmed Cell Death 1 Receptor</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012507" MajorTopicYN="N">Sarcoidosis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" 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Hawkins</name><name sortKey="Rotsinger, Joseph E" sort="Rotsinger, Joseph E" uniqKey="Rotsinger J" first="Joseph E" last="Rotsinger">Joseph E. Rotsinger</name><name sortKey="Shelton, Debresha" sort="Shelton, Debresha" uniqKey="Shelton D" first="Debresha" last="Shelton">Debresha Shelton</name><name sortKey="Young, Anjuli" sort="Young, Anjuli" uniqKey="Young A" first="Anjuli" last="Young">Anjuli Young</name></noCountry><country name="États-Unis"><region name="Tennessee"><name sortKey="Celada, Lindsay J" sort="Celada, Lindsay J" uniqKey="Celada L" first="Lindsay J" last="Celada">Lindsay J. Celada</name></region><name sortKey="Drake, Wonder P" sort="Drake, Wonder P" uniqKey="Drake W" first="Wonder P" last="Drake">Wonder P. Drake</name><name sortKey="Shaginurova, Guzel" sort="Shaginurova, Guzel" uniqKey="Shaginurova G" first="Guzel" last="Shaginurova">Guzel Shaginurova</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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