Regulation of MHC class I membrane expression by beta 2-microglobulin.
Identifieur interne : 001154 ( Ncbi/Merge ); précédent : 001153; suivant : 001155Regulation of MHC class I membrane expression by beta 2-microglobulin.
Auteurs : U M Abdel Motal [Suède] ; M X Zhou ; A R Siddiqi ; M. JondalSource :
- Scandinavian journal of immunology [ 0300-9475 ] ; 1993.
Descripteurs français
- KwdFr :
- Animaux, Antibactériens (pharmacologie), Antigènes d'histocompatibilité de classe I (immunologie), Antigènes de surface (immunologie), Bréfeldine A, Cellules cancéreuses en culture, Chloroquine (pharmacologie), Cyclopentanes (pharmacologie), Cytométrie en flux, Données de séquences moléculaires, Humains, Lymphocytes T cytotoxiques (immunologie), Peptides (immunologie), Régulation positive (), Souris, Séquence d'acides aminés, bêta-2-Microglobuline (immunologie).
- MESH :
- immunologie : Antigènes d'histocompatibilité de classe I, Antigènes de surface, Lymphocytes T cytotoxiques, Peptides, bêta-2-Microglobuline.
- pharmacologie : Antibactériens, Chloroquine, Cyclopentanes.
- Animaux, Bréfeldine A, Cellules cancéreuses en culture, Cytométrie en flux, Données de séquences moléculaires, Humains, Régulation positive, Souris, Séquence d'acides aminés.
English descriptors
- KwdEn :
- Amino Acid Sequence, Animals, Anti-Bacterial Agents (pharmacology), Antigens, Surface (immunology), Brefeldin A, Chloroquine (pharmacology), Cyclopentanes (pharmacology), Flow Cytometry, Histocompatibility Antigens Class I (immunology), Humans, Mice, Molecular Sequence Data, Peptides (immunology), T-Lymphocytes, Cytotoxic (immunology), Tumor Cells, Cultured, Up-Regulation (drug effects), beta 2-Microglobulin (immunology).
- MESH :
- chemical , immunology : Antigens, Surface, Histocompatibility Antigens Class I, Peptides, beta 2-Microglobulin.
- chemical , pharmacology : Anti-Bacterial Agents, Chloroquine, Cyclopentanes.
- drug effects : Up-Regulation.
- immunology : T-Lymphocytes, Cytotoxic.
- Amino Acid Sequence, Animals, Brefeldin A, Flow Cytometry, Humans, Mice, Molecular Sequence Data, Tumor Cells, Cultured.
Abstract
MHC-I binding peptides and beta 2 microglobulin (beta 2-m) can upregulate the MHC-I heavy chain expression on certain peptide transporter mutant cells. We have further studied this with normal cells and non-mutant cell lines. No MHC-I upregulation was seen with normal, resting or activated T cells. On mouse cell lines P815 and B16, both peptides and human beta 2-m gave an additive upregulation response. With the human small cell lung carcinoma H82, an optimal HLA.A2 binding peptide (GILGFVFTL) gave an upregulation response, whereas beta 2-m alone or in combination with this peptide had no effect. However, beta 2-m potentiated the response of H82 cells to a slightly longer peptide. Using mutant RMA-S cells, it was found that both Brefeldin A (BFA) and chloroquine, but not leupeptin, inhibited MHC-I upregulation response to both peptide and beta 2-m. In contrast to chloroquine, BFA also gave a reduction of background membrane MHC-I expression, presumably due to a block in Golgi transport. Human beta 2-m, which binds to RMA-S cells, and which is known to internalize into endosomes, did not reappear on the cell surface. When Db on RMA-S cells was upregulated by human beta 2-m, the sensitivity of these cells to Db restricted CTL cells increased. Even if beta 2-m did not upregulate the overall MHC-I expression on normal cells, it may still quantitatively increase the expression of optimally presented peptides and endosomal recycling many be important in this process.
DOI: 10.1111/j.1365-3083.1993.tb01743.x
PubMed: 8211001
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Jondal</name></author></analytic><series><title level="j">Scandinavian journal of immunology</title><idno type="ISSN">0300-9475</idno><imprint><date when="1993" type="published">1993</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Anti-Bacterial Agents (pharmacology)</term><term>Antigens, Surface (immunology)</term><term>Brefeldin A</term><term>Chloroquine (pharmacology)</term><term>Cyclopentanes (pharmacology)</term><term>Flow Cytometry</term><term>Histocompatibility Antigens Class I (immunology)</term><term>Humans</term><term>Mice</term><term>Molecular Sequence Data</term><term>Peptides (immunology)</term><term>T-Lymphocytes, Cytotoxic (immunology)</term><term>Tumor Cells, Cultured</term><term>Up-Regulation (drug effects)</term><term>beta 2-Microglobulin (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antibactériens (pharmacologie)</term><term>Antigènes d'histocompatibilité de classe I (immunologie)</term><term>Antigènes de surface (immunologie)</term><term>Bréfeldine A</term><term>Cellules cancéreuses en culture</term><term>Chloroquine (pharmacologie)</term><term>Cyclopentanes (pharmacologie)</term><term>Cytométrie en flux</term><term>Données de séquences moléculaires</term><term>Humains</term><term>Lymphocytes T cytotoxiques (immunologie)</term><term>Peptides (immunologie)</term><term>Régulation positive ()</term><term>Souris</term><term>Séquence d'acides aminés</term><term>bêta-2-Microglobuline (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antigens, Surface</term><term>Histocompatibility Antigens Class I</term><term>Peptides</term><term>beta 2-Microglobulin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Bacterial Agents</term><term>Chloroquine</term><term>Cyclopentanes</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Up-Regulation</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Antigènes d'histocompatibilité de classe I</term><term>Antigènes de surface</term><term>Lymphocytes T cytotoxiques</term><term>Peptides</term><term>bêta-2-Microglobuline</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>T-Lymphocytes, Cytotoxic</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antibactériens</term><term>Chloroquine</term><term>Cyclopentanes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Brefeldin A</term><term>Flow Cytometry</term><term>Humans</term><term>Mice</term><term>Molecular Sequence Data</term><term>Tumor Cells, Cultured</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Bréfeldine A</term><term>Cellules cancéreuses en culture</term><term>Cytométrie en flux</term><term>Données de séquences moléculaires</term><term>Humains</term><term>Régulation positive</term><term>Souris</term><term>Séquence d'acides aminés</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">MHC-I binding peptides and beta 2 microglobulin (beta 2-m) can upregulate the MHC-I heavy chain expression on certain peptide transporter mutant cells. We have further studied this with normal cells and non-mutant cell lines. No MHC-I upregulation was seen with normal, resting or activated T cells. On mouse cell lines P815 and B16, both peptides and human beta 2-m gave an additive upregulation response. With the human small cell lung carcinoma H82, an optimal HLA.A2 binding peptide (GILGFVFTL) gave an upregulation response, whereas beta 2-m alone or in combination with this peptide had no effect. However, beta 2-m potentiated the response of H82 cells to a slightly longer peptide. Using mutant RMA-S cells, it was found that both Brefeldin A (BFA) and chloroquine, but not leupeptin, inhibited MHC-I upregulation response to both peptide and beta 2-m. In contrast to chloroquine, BFA also gave a reduction of background membrane MHC-I expression, presumably due to a block in Golgi transport. Human beta 2-m, which binds to RMA-S cells, and which is known to internalize into endosomes, did not reappear on the cell surface. When Db on RMA-S cells was upregulated by human beta 2-m, the sensitivity of these cells to Db restricted CTL cells increased. Even if beta 2-m did not upregulate the overall MHC-I expression on normal cells, it may still quantitatively increase the expression of optimally presented peptides and endosomal recycling many be important in this process.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8211001</PMID><DateCompleted><Year>1993</Year><Month>11</Month><Day>15</Day></DateCompleted><DateRevised><Year>2019</Year><Month>08</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0300-9475</ISSN><JournalIssue CitedMedium="Print"><Volume>38</Volume><Issue>4</Issue><PubDate><Year>1993</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Scandinavian journal of immunology</Title><ISOAbbreviation>Scand. J. 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Using mutant RMA-S cells, it was found that both Brefeldin A (BFA) and chloroquine, but not leupeptin, inhibited MHC-I upregulation response to both peptide and beta 2-m. In contrast to chloroquine, BFA also gave a reduction of background membrane MHC-I expression, presumably due to a block in Golgi transport. Human beta 2-m, which binds to RMA-S cells, and which is known to internalize into endosomes, did not reappear on the cell surface. When Db on RMA-S cells was upregulated by human beta 2-m, the sensitivity of these cells to Db restricted CTL cells increased. 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PubStatus="pubmed"><Year>1993</Year><Month>10</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1993</Year><Month>10</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1993</Year><Month>10</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8211001</ArticleId><ArticleId IdType="doi">10.1111/j.1365-3083.1993.tb01743.x</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Suède</li></country><region><li>Svealand</li></region><settlement><li>Stockholm</li></settlement></list><tree><noCountry><name sortKey="Jondal, M" sort="Jondal, M" uniqKey="Jondal M" first="M" last="Jondal">M. Jondal</name><name sortKey="Siddiqi, A R" sort="Siddiqi, A R" uniqKey="Siddiqi A" first="A R" last="Siddiqi">A R Siddiqi</name><name sortKey="Zhou, M X" sort="Zhou, M X" uniqKey="Zhou M" first="M X" last="Zhou">M X Zhou</name></noCountry><country name="Suède"><region name="Svealand"><name sortKey="Abdel Motal, U M" sort="Abdel Motal, U M" uniqKey="Abdel Motal U" first="U M" last="Abdel Motal">U M Abdel Motal</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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