Regulation of MHC class I membrane expression by beta 2-microglobulin.
Identifieur interne : 000534 ( PubMed/Curation ); précédent : 000533; suivant : 000535Regulation 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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pubmed:8211001Le document en format XML
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<term>Antigens, Surface (immunology)</term>
<term>Brefeldin A</term>
<term>Chloroquine (pharmacology)</term>
<term>Cyclopentanes (pharmacology)</term>
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<term>Histocompatibility Antigens Class I (immunology)</term>
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<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>
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<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>
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<term>Histocompatibility Antigens Class I</term>
<term>Peptides</term>
<term>beta 2-Microglobulin</term>
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<term>Chloroquine</term>
<term>Cyclopentanes</term>
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<term>Antigènes de surface</term>
<term>Lymphocytes T cytotoxiques</term>
<term>Peptides</term>
<term>bêta-2-Microglobuline</term>
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<term>Animals</term>
<term>Brefeldin A</term>
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<term>Humans</term>
<term>Mice</term>
<term>Molecular Sequence Data</term>
<term>Tumor Cells, Cultured</term>
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<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>
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<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>
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<Abstract><AbstractText>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.</AbstractText>
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