Stress-induced modulation of antigen-presenting cell function.
Identifieur interne : 000A32 ( PubMed/Checkpoint ); précédent : 000A31; suivant : 000A33Stress-induced modulation of antigen-presenting cell function.
Auteurs : A D Rees [Royaume-Uni] ; Y. Donati ; G. Lombardi ; J. Lamb ; B. Polla ; R. LechlerSource :
- Immunology [ 0019-2805 ] ; 1991.
Descripteurs français
- KwdFr :
- Antigène HLA-DR1 (immunologie), Antigènes HLA-D (analyse), Cellules cultivées, Cellules présentatrices d'antigène (immunologie), Coopération des lymphocytes (immunologie), Division cellulaire (immunologie), Humains, Lignée cellulaire, Lymphocytes B (immunologie), Lymphocytes T (immunologie), Peroxyde d'hydrogène, Stress physiologique (immunologie), Température élevée.
- MESH :
English descriptors
- KwdEn :
- Antigen-Presenting Cells (immunology), B-Lymphocytes (immunology), Cell Division (immunology), Cell Line, Cells, Cultured, HLA-D Antigens (analysis), HLA-DR1 Antigen (immunology), Hot Temperature, Humans, Hydrogen Peroxide, Lymphocyte Cooperation (immunology), Stress, Physiological (immunology), T-Lymphocytes (immunology).
- MESH :
- chemical , analysis : HLA-D Antigens.
- immunology : Antigen-Presenting Cells, B-Lymphocytes, Cell Division, HLA-DR1 Antigen, Lymphocyte Cooperation, Stress, Physiological, T-Lymphocytes.
- Cell Line, Cells, Cultured, Hot Temperature, Humans, Hydrogen Peroxide.
Abstract
The effect of two means of inducing a stress response, heat and oxygen radicals, on the ability of an HLA-DR1 B-cell line to stimulate DR1-restricted and anti-DR1 auto- and alloreactive T-cell clones has been examined. Both forms of stress enhanced the ability of B cells to stimulate auto- and alloreactive T-cell clones and to present peptide to an influenza-virus specific T-cell clone. Furthermore, the ability of the B-cell line to present whole influenza virus was augmented by heat stress. The stress-induced enhancement of T-cell responses coincided with a modest increase in the cell-surface expression of major histocompatibility class II products. This was, however, insufficient to account for the observed functional effects. In contrast to these effects, presentation of whole antigen was inhibited by the oxygen radical intermediate, hydrogen peroxide (peroxide), in a dose-dependent manner. When analysed by SDS-PAGE, it was found that whilst overall protein synthesis decreased following both types of stress, increased synthesis of heat-shock proteins (HSP), and in particular the 70,000 MW HSP, was only evident following heat stress. The absence of an increase in the synthesis of HSP 70, in the antigen-presenting cells (APC) following the uptake of UV-treated influenza virus, however, implied that HSP 70 induction was not necessary for the presentation of whole antigen. The effects of peroxide stress appeared to be qualitatively different in several respects. First, peroxide treatment did not cause the induction of any stress proteins; second, peroxide abolished the presentation of whole antigen. In addition, heat stress of APC was unable to protect from the adverse effects of peroxide treatment, in that cells treated sequentially with heat, followed by peroxide, were unable to present whole influenza virus. In order to determine the stage of antigen presentation at which peroxide was causing inhibition, APC were treated at varying time-points after pulsing with antigen. The kinetics of the peroxide effect paralleled those of aldehyde fixation. Taking these results together it would appear that peroxide interferes with some aspects of the antigen-processing pathway.
PubMed: 1769687
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Donati</name></author><author><name sortKey="Lombardi, G" sort="Lombardi, G" uniqKey="Lombardi G" first="G" last="Lombardi">G. Lombardi</name></author><author><name sortKey="Lamb, J" sort="Lamb, J" uniqKey="Lamb J" first="J" last="Lamb">J. Lamb</name></author><author><name sortKey="Polla, B" sort="Polla, B" uniqKey="Polla B" first="B" last="Polla">B. Polla</name></author><author><name sortKey="Lechler, R" sort="Lechler, R" uniqKey="Lechler R" first="R" last="Lechler">R. Lechler</name></author></analytic><series><title level="j">Immunology</title><idno type="ISSN">0019-2805</idno><imprint><date when="1991" type="published">1991</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigen-Presenting Cells (immunology)</term><term>B-Lymphocytes (immunology)</term><term>Cell Division (immunology)</term><term>Cell Line</term><term>Cells, Cultured</term><term>HLA-D Antigens (analysis)</term><term>HLA-DR1 Antigen (immunology)</term><term>Hot Temperature</term><term>Humans</term><term>Hydrogen Peroxide</term><term>Lymphocyte Cooperation (immunology)</term><term>Stress, Physiological (immunology)</term><term>T-Lymphocytes (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antigène HLA-DR1 (immunologie)</term><term>Antigènes HLA-D (analyse)</term><term>Cellules cultivées</term><term>Cellules présentatrices d'antigène (immunologie)</term><term>Coopération des lymphocytes (immunologie)</term><term>Division cellulaire (immunologie)</term><term>Humains</term><term>Lignée cellulaire</term><term>Lymphocytes B (immunologie)</term><term>Lymphocytes T (immunologie)</term><term>Peroxyde d'hydrogène</term><term>Stress physiologique (immunologie)</term><term>Température élevée</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>HLA-D Antigens</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Antigènes HLA-D</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Antigène HLA-DR1</term><term>Cellules présentatrices d'antigène</term><term>Coopération des lymphocytes</term><term>Division cellulaire</term><term>Lymphocytes B</term><term>Lymphocytes T</term><term>Stress physiologique</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Antigen-Presenting Cells</term><term>B-Lymphocytes</term><term>Cell Division</term><term>HLA-DR1 Antigen</term><term>Lymphocyte Cooperation</term><term>Stress, Physiological</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Cells, Cultured</term><term>Hot Temperature</term><term>Humans</term><term>Hydrogen Peroxide</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules cultivées</term><term>Humains</term><term>Lignée cellulaire</term><term>Peroxyde d'hydrogène</term><term>Température élevée</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The effect of two means of inducing a stress response, heat and oxygen radicals, on the ability of an HLA-DR1 B-cell line to stimulate DR1-restricted and anti-DR1 auto- and alloreactive T-cell clones has been examined. Both forms of stress enhanced the ability of B cells to stimulate auto- and alloreactive T-cell clones and to present peptide to an influenza-virus specific T-cell clone. Furthermore, the ability of the B-cell line to present whole influenza virus was augmented by heat stress. The stress-induced enhancement of T-cell responses coincided with a modest increase in the cell-surface expression of major histocompatibility class II products. This was, however, insufficient to account for the observed functional effects. In contrast to these effects, presentation of whole antigen was inhibited by the oxygen radical intermediate, hydrogen peroxide (peroxide), in a dose-dependent manner. When analysed by SDS-PAGE, it was found that whilst overall protein synthesis decreased following both types of stress, increased synthesis of heat-shock proteins (HSP), and in particular the 70,000 MW HSP, was only evident following heat stress. The absence of an increase in the synthesis of HSP 70, in the antigen-presenting cells (APC) following the uptake of UV-treated influenza virus, however, implied that HSP 70 induction was not necessary for the presentation of whole antigen. The effects of peroxide stress appeared to be qualitatively different in several respects. First, peroxide treatment did not cause the induction of any stress proteins; second, peroxide abolished the presentation of whole antigen. In addition, heat stress of APC was unable to protect from the adverse effects of peroxide treatment, in that cells treated sequentially with heat, followed by peroxide, were unable to present whole influenza virus. In order to determine the stage of antigen presentation at which peroxide was causing inhibition, APC were treated at varying time-points after pulsing with antigen. The kinetics of the peroxide effect paralleled those of aldehyde fixation. Taking these results together it would appear that peroxide interferes with some aspects of the antigen-processing pathway.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1769687</PMID><DateCompleted><Year>1992</Year><Month>02</Month><Day>26</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0019-2805</ISSN><JournalIssue CitedMedium="Print"><Volume>74</Volume><Issue>3</Issue><PubDate><Year>1991</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Immunology</Title><ISOAbbreviation>Immunology</ISOAbbreviation></Journal><ArticleTitle>Stress-induced modulation of antigen-presenting cell function.</ArticleTitle><Pagination><MedlinePgn>386-92</MedlinePgn></Pagination><Abstract><AbstractText>The effect of two means of inducing a stress response, heat and oxygen radicals, on the ability of an HLA-DR1 B-cell line to stimulate DR1-restricted and anti-DR1 auto- and alloreactive T-cell clones has been examined. Both forms of stress enhanced the ability of B cells to stimulate auto- and alloreactive T-cell clones and to present peptide to an influenza-virus specific T-cell clone. Furthermore, the ability of the B-cell line to present whole influenza virus was augmented by heat stress. The stress-induced enhancement of T-cell responses coincided with a modest increase in the cell-surface expression of major histocompatibility class II products. This was, however, insufficient to account for the observed functional effects. In contrast to these effects, presentation of whole antigen was inhibited by the oxygen radical intermediate, hydrogen peroxide (peroxide), in a dose-dependent manner. When analysed by SDS-PAGE, it was found that whilst overall protein synthesis decreased following both types of stress, increased synthesis of heat-shock proteins (HSP), and in particular the 70,000 MW HSP, was only evident following heat stress. The absence of an increase in the synthesis of HSP 70, in the antigen-presenting cells (APC) following the uptake of UV-treated influenza virus, however, implied that HSP 70 induction was not necessary for the presentation of whole antigen. The effects of peroxide stress appeared to be qualitatively different in several respects. First, peroxide treatment did not cause the induction of any stress proteins; second, peroxide abolished the presentation of whole antigen. In addition, heat stress of APC was unable to protect from the adverse effects of peroxide treatment, in that cells treated sequentially with heat, followed by peroxide, were unable to present whole influenza virus. In order to determine the stage of antigen presentation at which peroxide was causing inhibition, APC were treated at varying time-points after pulsing with antigen. The kinetics of the peroxide effect paralleled those of aldehyde fixation. Taking these results together it would appear that peroxide interferes with some aspects of the antigen-processing pathway.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rees</LastName><ForeName>A D</ForeName><Initials>AD</Initials><AffiliationInfo><Affiliation>MRC Tuberculosis & Related Infections Unit, Hammersmith Hospital, London, U.K.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Donati</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Lombardi</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Lamb</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Polla</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Lechler</LastName><ForeName>R</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType 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PubStatus="medline"><Year>1991</Year><Month>11</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1991</Year><Month>11</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1769687</ArticleId><ArticleId IdType="pmc">PMC1384629</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Int Immunol. 1989;1(5):479-86</Citation><ArticleIdList><ArticleId IdType="pubmed">2489038</ArticleId></ArticleIdList></Reference><Reference><Citation>J Exp Med. 1979 Jan 1;149(1):84-99</Citation><ArticleIdList><ArticleId IdType="pubmed">368287</ArticleId></ArticleIdList></Reference><Reference><Citation>Int Immunol. 1989;1(6):624-30</Citation><ArticleIdList><ArticleId IdType="pubmed">2489049</ArticleId></ArticleIdList></Reference><Reference><Citation>Semin Cell Biol. 1990 Feb;1(1):27-35</Citation><ArticleIdList><ArticleId IdType="pubmed">1983268</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 1989 Feb 1;142(3):753-9</Citation><ArticleIdList><ArticleId IdType="pubmed">2492329</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1988 May 26;333(6171):330-4</Citation><ArticleIdList><ArticleId IdType="pubmed">2897629</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 1985 Nov;135(5):2914-22</Citation><ArticleIdList><ArticleId IdType="pubmed">3900200</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1988 Nov;85(21):8191-5</Citation><ArticleIdList><ArticleId IdType="pubmed">2973061</ArticleId></ArticleIdList></Reference><Reference><Citation>FASEB J. 1987 Nov;1(5):358-64</Citation><ArticleIdList><ArticleId IdType="pubmed">2824268</ArticleId></ArticleIdList></Reference><Reference><Citation>J Exp Med. 1987 Feb 1;165(2):302-19</Citation><ArticleIdList><ArticleId IdType="pubmed">3029267</ArticleId></ArticleIdList></Reference><Reference><Citation>Annu Rev Biochem. 1986;55:1151-91</Citation><ArticleIdList><ArticleId IdType="pubmed">2427013</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1989 Mar;86(6):1968-72</Citation><ArticleIdList><ArticleId IdType="pubmed">2538825</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1989 Jun;86(11):4190-4</Citation><ArticleIdList><ArticleId IdType="pubmed">2657745</ArticleId></ArticleIdList></Reference><Reference><Citation>J Exp Med. 1989 Dec 1;170(6):1799-809</Citation><ArticleIdList><ArticleId IdType="pubmed">2584924</ArticleId></ArticleIdList></Reference><Reference><Citation>Science. 1989 Sep 8;245(4922):1112-5</Citation><ArticleIdList><ArticleId IdType="pubmed">2788923</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunol Today. 1988 May;9(5):134-7</Citation><ArticleIdList><ArticleId IdType="pubmed">3256318</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1985 Sep 26-Oct 2;317(6035):359-61</Citation><ArticleIdList><ArticleId IdType="pubmed">3876513</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1990 Aug 16;346(6285):655-7</Citation><ArticleIdList><ArticleId IdType="pubmed">2166918</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1990 Feb;87(3):1081-5</Citation><ArticleIdList><ArticleId IdType="pubmed">2153967</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 1990 Apr 15;144(8):2883-90</Citation><ArticleIdList><ArticleId IdType="pubmed">2139072</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1990 Aug 2;346(6283):476-80</Citation><ArticleIdList><ArticleId IdType="pubmed">2198471</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1982 Nov 4;300(5887):66-9</Citation><ArticleIdList><ArticleId IdType="pubmed">6982419</ArticleId></ArticleIdList></Reference><Reference><Citation>Chest. 1982 Sep;82(3):266-71</Citation><ArticleIdList><ArticleId IdType="pubmed">6980777</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 1980 Feb;124(2):983-8</Citation><ArticleIdList><ArticleId IdType="pubmed">7356724</ArticleId></ArticleIdList></Reference><Reference><Citation>Int Immunol. 1989;1(2):191-6</Citation><ArticleIdList><ArticleId IdType="pubmed">2484883</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><noCountry><name sortKey="Donati, Y" sort="Donati, Y" uniqKey="Donati Y" first="Y" last="Donati">Y. Donati</name><name sortKey="Lamb, J" sort="Lamb, J" uniqKey="Lamb J" first="J" last="Lamb">J. Lamb</name><name sortKey="Lechler, R" sort="Lechler, R" uniqKey="Lechler R" first="R" last="Lechler">R. Lechler</name><name sortKey="Lombardi, G" sort="Lombardi, G" uniqKey="Lombardi G" first="G" last="Lombardi">G. Lombardi</name><name sortKey="Polla, B" sort="Polla, B" uniqKey="Polla B" first="B" last="Polla">B. Polla</name></noCountry><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Rees, A D" sort="Rees, A D" uniqKey="Rees A" first="A D" last="Rees">A D Rees</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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