Severe acute respiratory syndrome and the innate immune responses: modulation of effector cell function without productive infection.
Identifieur interne : 004635 ( Main/Exploration ); précédent : 004634; suivant : 004636Severe acute respiratory syndrome and the innate immune responses: modulation of effector cell function without productive infection.
Auteurs : Chien-Te K. Tseng [États-Unis] ; Lucy A. Perrone ; Hongbing Zhu ; Shinji Makino ; Clarence J. PetersSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 2005.
Descripteurs français
- KwdFr :
- Activation des lymphocytes (immunologie), Cellules U937, Cellules dendritiques (cytologie), Cellules dendritiques (immunologie), Cellules dendritiques (métabolisme), Cellules dendritiques (virologie), Différenciation cellulaire (immunologie), Endocytose (immunologie), Humains, Immunité cellulaire, Immunité innée, Immunophénotypage, Interleukine-12 (biosynthèse), Interleukine-6 (biosynthèse), Lectines de type C (antagonistes et inhibiteurs), Lectines de type C (physiologie), Lectines liant le mannose (antagonistes et inhibiteurs), Lectines liant le mannose (physiologie), Lignée cellulaire, Macrophages (cytologie), Macrophages (immunologie), Macrophages (métabolisme), Macrophages (virologie), Mort cellulaire (immunologie), Récepteurs de surface cellulaire (antagonistes et inhibiteurs), Récepteurs de surface cellulaire (physiologie), Susceptibilité à une maladie, Syndrome respiratoire aigu sévère (immunologie), Virus du SRAS (immunologie), Virus du SRAS (pathogénicité).
- MESH :
- antagonistes et inhibiteurs : Lectines de type C, Lectines liant le mannose, Récepteurs de surface cellulaire.
- biosynthèse : Interleukine-12, Interleukine-6.
- cytologie : Cellules dendritiques, Macrophages.
- immunologie : Activation des lymphocytes, Cellules dendritiques, Différenciation cellulaire, Endocytose, Macrophages, Mort cellulaire, Syndrome respiratoire aigu sévère, Virus du SRAS.
- métabolisme : Cellules dendritiques, Macrophages.
- pathogénicité : Virus du SRAS.
- physiologie : Lectines de type C, Lectines liant le mannose, Récepteurs de surface cellulaire.
- virologie : Cellules dendritiques, Macrophages.
- Cellules U937, Humains, Immunité cellulaire, Immunité innée, Immunophénotypage, Lignée cellulaire, Susceptibilité à une maladie.
English descriptors
- KwdEn :
- Cell Death (immunology), Cell Differentiation (immunology), Cell Line, Dendritic Cells (cytology), Dendritic Cells (immunology), Dendritic Cells (metabolism), Dendritic Cells (virology), Disease Susceptibility, Endocytosis (immunology), Humans, Immunity, Cellular, Immunity, Innate, Immunophenotyping, Interleukin-12 (biosynthesis), Interleukin-6 (biosynthesis), Lectins, C-Type (antagonists & inhibitors), Lectins, C-Type (physiology), Lymphocyte Activation (immunology), Macrophages (cytology), Macrophages (immunology), Macrophages (metabolism), Macrophages (virology), Mannose-Binding Lectins (antagonists & inhibitors), Mannose-Binding Lectins (physiology), Receptors, Cell Surface (antagonists & inhibitors), Receptors, Cell Surface (physiology), SARS Virus (immunology), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (immunology), U937 Cells.
- MESH :
- chemical , antagonists & inhibitors : Lectins, C-Type, Mannose-Binding Lectins, Receptors, Cell Surface.
- chemical , biosynthesis : Interleukin-12, Interleukin-6.
- cytology : Dendritic Cells, Macrophages.
- immunology : Cell Death, Cell Differentiation, Dendritic Cells, Endocytosis, Lymphocyte Activation, Macrophages, SARS Virus, Severe Acute Respiratory Syndrome.
- metabolism : Dendritic Cells, Macrophages.
- pathogenicity : SARS Virus.
- chemical , physiology : Lectins, C-Type, Mannose-Binding Lectins, Receptors, Cell Surface.
- virology : Dendritic Cells, Macrophages.
- Cell Line, Disease Susceptibility, Humans, Immunity, Cellular, Immunity, Innate, Immunophenotyping, U937 Cells.
Abstract
Severe acute respiratory syndrome (SARS) caused by a novel human coronavirus (CoV), designated SARS-CoV, is a highly contagious respiratory disease with the lungs as a major target. Although the exact mechanism of SARS-CoV pathogenesis remains unknown, an intense, ill-regulated local inflammatory response has been suggested as partially responsible for the devastating lung pathology. We investigated the interaction of SARS-CoV with human macrophages (Mphi) and dendritic cells (DC), two key innate immune cells of the host immune system, by focusing on their susceptibility to viral infection and subsequent responses (e.g., phenotypic maturation, T cell-priming activity, phagocytosis, and cytokine production). We found neither cell to be permissive for SARS-CoV replication. However, incubation of Mphi and DC with live, but not gamma irradiation-inactivated, viruses appeared to better sustain their viability. Also, exposure to infectious SARS-CoV led to the phenotypic and functional maturation of DC, with regard to MHC class II and costimulatory molecule expression, T cell-stimulatory capacity, and cytokine production, respectively. Cytokine production was also observed for Mphi, which were refractory to cell surface phenotypic changes. Strikingly, live SARS-CoV could further prime cell types to respond to a suboptimal dose of bacterial LPS (100 ng/ml), resulting in massive release of IL-6 and IL-12. However, the endocytic capacity (e.g., Ag capture) of Mphi was significantly compromised upon exposure to infectious SARS-CoV. This study is the first demonstration that although SARS-CoV does not productively infect human Mphi or DC, it appears to exert differential effects on Mphi and DC maturation and functions, which might contribute to SARS pathogenesis.
DOI: 10.4049/jimmunol.174.12.7977
PubMed: 15944304
Affiliations:
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Perrone</name></author><author><name sortKey="Zhu, Hongbing" sort="Zhu, Hongbing" uniqKey="Zhu H" first="Hongbing" last="Zhu">Hongbing Zhu</name></author><author><name sortKey="Makino, Shinji" sort="Makino, Shinji" uniqKey="Makino S" first="Shinji" last="Makino">Shinji Makino</name></author><author><name sortKey="Peters, Clarence J" sort="Peters, Clarence J" uniqKey="Peters C" first="Clarence J" last="Peters">Clarence J. 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Tseng</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA. sktseng@utmb.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Perrone, Lucy A" sort="Perrone, Lucy A" uniqKey="Perrone L" first="Lucy A" last="Perrone">Lucy A. Perrone</name></author><author><name sortKey="Zhu, Hongbing" sort="Zhu, Hongbing" uniqKey="Zhu H" first="Hongbing" last="Zhu">Hongbing Zhu</name></author><author><name sortKey="Makino, Shinji" sort="Makino, Shinji" uniqKey="Makino S" first="Shinji" last="Makino">Shinji Makino</name></author><author><name sortKey="Peters, Clarence J" sort="Peters, Clarence J" uniqKey="Peters C" first="Clarence J" last="Peters">Clarence J. Peters</name></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="ISSN">0022-1767</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Death (immunology)</term><term>Cell Differentiation (immunology)</term><term>Cell Line</term><term>Dendritic Cells (cytology)</term><term>Dendritic Cells (immunology)</term><term>Dendritic Cells (metabolism)</term><term>Dendritic Cells (virology)</term><term>Disease Susceptibility</term><term>Endocytosis (immunology)</term><term>Humans</term><term>Immunity, Cellular</term><term>Immunity, Innate</term><term>Immunophenotyping</term><term>Interleukin-12 (biosynthesis)</term><term>Interleukin-6 (biosynthesis)</term><term>Lectins, C-Type (antagonists & inhibitors)</term><term>Lectins, C-Type (physiology)</term><term>Lymphocyte Activation (immunology)</term><term>Macrophages (cytology)</term><term>Macrophages (immunology)</term><term>Macrophages (metabolism)</term><term>Macrophages (virology)</term><term>Mannose-Binding Lectins (antagonists & inhibitors)</term><term>Mannose-Binding Lectins (physiology)</term><term>Receptors, Cell Surface (antagonists & inhibitors)</term><term>Receptors, Cell Surface (physiology)</term><term>SARS Virus (immunology)</term><term>SARS Virus (pathogenicity)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>U937 Cells</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation des lymphocytes (immunologie)</term><term>Cellules U937</term><term>Cellules dendritiques (cytologie)</term><term>Cellules dendritiques (immunologie)</term><term>Cellules dendritiques (métabolisme)</term><term>Cellules dendritiques (virologie)</term><term>Différenciation cellulaire (immunologie)</term><term>Endocytose (immunologie)</term><term>Humains</term><term>Immunité cellulaire</term><term>Immunité innée</term><term>Immunophénotypage</term><term>Interleukine-12 (biosynthèse)</term><term>Interleukine-6 (biosynthèse)</term><term>Lectines de type C (antagonistes et inhibiteurs)</term><term>Lectines de type C (physiologie)</term><term>Lectines liant le mannose (antagonistes et inhibiteurs)</term><term>Lectines liant le mannose (physiologie)</term><term>Lignée cellulaire</term><term>Macrophages (cytologie)</term><term>Macrophages (immunologie)</term><term>Macrophages (métabolisme)</term><term>Macrophages (virologie)</term><term>Mort cellulaire (immunologie)</term><term>Récepteurs de surface cellulaire (antagonistes et inhibiteurs)</term><term>Récepteurs de surface cellulaire (physiologie)</term><term>Susceptibilité à une maladie</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Virus du SRAS (immunologie)</term><term>Virus du SRAS (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Lectins, C-Type</term><term>Mannose-Binding Lectins</term><term>Receptors, Cell Surface</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interleukin-12</term><term>Interleukin-6</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Lectines de type C</term><term>Lectines liant le mannose</term><term>Récepteurs de surface cellulaire</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Interleukine-12</term><term>Interleukine-6</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules dendritiques</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Dendritic Cells</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Activation des lymphocytes</term><term>Cellules 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qualifier="physiologie" xml:lang="fr"><term>Lectines de type C</term><term>Lectines liant le mannose</term><term>Récepteurs de surface cellulaire</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Lectins, C-Type</term><term>Mannose-Binding Lectins</term><term>Receptors, Cell Surface</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Cellules dendritiques</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Dendritic Cells</term><term>Macrophages</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Disease Susceptibility</term><term>Humans</term><term>Immunity, Cellular</term><term>Immunity, Innate</term><term>Immunophenotyping</term><term>U937 Cells</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules U937</term><term>Humains</term><term>Immunité cellulaire</term><term>Immunité innée</term><term>Immunophénotypage</term><term>Lignée cellulaire</term><term>Susceptibilité à une maladie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) caused by a novel human coronavirus (CoV), designated SARS-CoV, is a highly contagious respiratory disease with the lungs as a major target. Although the exact mechanism of SARS-CoV pathogenesis remains unknown, an intense, ill-regulated local inflammatory response has been suggested as partially responsible for the devastating lung pathology. We investigated the interaction of SARS-CoV with human macrophages (Mphi) and dendritic cells (DC), two key innate immune cells of the host immune system, by focusing on their susceptibility to viral infection and subsequent responses (e.g., phenotypic maturation, T cell-priming activity, phagocytosis, and cytokine production). We found neither cell to be permissive for SARS-CoV replication. However, incubation of Mphi and DC with live, but not gamma irradiation-inactivated, viruses appeared to better sustain their viability. Also, exposure to infectious SARS-CoV led to the phenotypic and functional maturation of DC, with regard to MHC class II and costimulatory molecule expression, T cell-stimulatory capacity, and cytokine production, respectively. Cytokine production was also observed for Mphi, which were refractory to cell surface phenotypic changes. Strikingly, live SARS-CoV could further prime cell types to respond to a suboptimal dose of bacterial LPS (100 ng/ml), resulting in massive release of IL-6 and IL-12. However, the endocytic capacity (e.g., Ag capture) of Mphi was significantly compromised upon exposure to infectious SARS-CoV. This study is the first demonstration that although SARS-CoV does not productively infect human Mphi or DC, it appears to exert differential effects on Mphi and DC maturation and functions, which might contribute to SARS pathogenesis.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Texas</li></region></list><tree><noCountry><name sortKey="Makino, Shinji" sort="Makino, Shinji" uniqKey="Makino S" first="Shinji" last="Makino">Shinji Makino</name><name sortKey="Perrone, Lucy A" sort="Perrone, Lucy A" uniqKey="Perrone L" first="Lucy A" last="Perrone">Lucy A. Perrone</name><name sortKey="Peters, Clarence J" sort="Peters, Clarence J" uniqKey="Peters C" first="Clarence J" last="Peters">Clarence J. Peters</name><name sortKey="Zhu, Hongbing" sort="Zhu, Hongbing" uniqKey="Zhu H" first="Hongbing" last="Zhu">Hongbing Zhu</name></noCountry><country name="États-Unis"><region name="Texas"><name sortKey="Tseng, Chien Te K" sort="Tseng, Chien Te K" uniqKey="Tseng C" first="Chien-Te K" last="Tseng">Chien-Te K. Tseng</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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