Staphylococcal enterotoxin-mediated human T-T cell interactions.
Identifieur interne : 000160 ( Main/Curation ); précédent : 000159; suivant : 000161Staphylococcal enterotoxin-mediated human T-T cell interactions.
Auteurs : F. Koning [Pays-Bas] ; C. RustSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 1992.
Descripteurs français
- KwdFr :
- Activation des lymphocytes (MeSH), Antigènes bactériens (immunologie), Clones cellulaires (MeSH), Coopération des lymphocytes (MeSH), Cytotoxicité immunologique (MeSH), Entérotoxines (immunologie), Humains (MeSH), Immunité cellulaire (MeSH), Récepteur lymphocytaire T antigène, alpha-bêta (immunologie), Récepteur lymphocytaire T antigène, gamma-delta (immunologie), Sous-populations de lymphocytes T (immunologie), Staphylococcus aureus (immunologie), Techniques in vitro (MeSH).
- MESH :
- immunologie : Antigènes bactériens, Entérotoxines, Récepteur lymphocytaire T antigène, alpha-bêta, Récepteur lymphocytaire T antigène, gamma-delta, Sous-populations de lymphocytes T, Staphylococcus aureus.
- Activation des lymphocytes, Clones cellulaires, Coopération des lymphocytes, Cytotoxicité immunologique, Humains, Immunité cellulaire, Techniques in vitro.
English descriptors
- KwdEn :
- Antigens, Bacterial (immunology), Clone Cells (MeSH), Cytotoxicity, Immunologic (MeSH), Enterotoxins (immunology), Humans (MeSH), Immunity, Cellular (MeSH), In Vitro Techniques (MeSH), Lymphocyte Activation (MeSH), Lymphocyte Cooperation (MeSH), Receptors, Antigen, T-Cell, alpha-beta (immunology), Receptors, Antigen, T-Cell, gamma-delta (immunology), Staphylococcus aureus (immunology), T-Lymphocyte Subsets (immunology).
- MESH :
- chemical , immunology : Antigens, Bacterial, Enterotoxins, Receptors, Antigen, T-Cell, alpha-beta, Receptors, Antigen, T-Cell, gamma-delta.
- immunology : Staphylococcus aureus, T-Lymphocyte Subsets.
- Clone Cells, Cytotoxicity, Immunologic, Humans, Immunity, Cellular, In Vitro Techniques, Lymphocyte Activation, Lymphocyte Cooperation.
Abstract
Staphylococcal enterotoxins (SE) are known to stimulate a large proportion of T cells. SE bind to MHC-class II molecules on APC and a particular segment of certain TCR V beta and V gamma gene products. Resting human T cells do not express HLA class II Ag and therefore cannot present SE to T cells. Activated human T cells, however, do express HLA-DR, -DP, and -DQ Ag and could consequently serve as APC for SE. As such, local immune responses to SE might be regulated and/or abrogated by SE-mediated T-T cell interactions leading to T cell destruction. We have investigated if such SE-mediated T-T cell interactions can occur in vitro using human cytolytic TCR-alpha beta+ and TCR-gamma delta+ T cell clones. We demonstrate that the TCR-alpha beta+ T cell clones can efficiently present staphylococcal enterotoxin A (SEA) to each other: T cell clones coated with SEA are lysed by SEA-reactive T cell clones but not by a SEA-nonreactive T cell clone. Furthermore, the SEA-reactive TCR-alpha beta+ clones (but not the SEA-nonreactive clone) destruct themselves in the presence of SEA at low concentrations of SEA (less than 0.01 microgram/ml). Also, SEA-coated T cell clones can induce proliferative responses although such responses are much weaker than those induced when B cells are used as stimulator cells. In contrast, the SEA-reactive TCR-gamma delta+ T cell clones are resistant to autokilling in the presence of SEA and they do not lyse SEA-coated TCR-gamma delta+ targets. However, such targets can be lysed by TCR-alpha beta+ effector cells. These results indicate that TCR-gamma delta+ cells are relatively resistant to lysis and that during local nonspecific immune responses triggered by SE, which induces HLA-class II expression by the responding T cells, SE-mediated T-T cell interactions may play a role in the regulation and/or abrogation of these immune responses.
PubMed: 1535087
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<author><name sortKey="Koning, F" sort="Koning, F" uniqKey="Koning F" first="F" last="Koning">F. Koning</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunohematology and Bloodbank, University Hospital, Leiden, The Netherlands.</nlm:affiliation>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Immunohematology and Bloodbank, University Hospital, Leiden</wicri:regionArea>
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<author><name sortKey="Rust, C" sort="Rust, C" uniqKey="Rust C" first="C" last="Rust">C. Rust</name>
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<author><name sortKey="Koning, F" sort="Koning, F" uniqKey="Koning F" first="F" last="Koning">F. Koning</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunohematology and Bloodbank, University Hospital, Leiden, The Netherlands.</nlm:affiliation>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigens, Bacterial (immunology)</term>
<term>Clone Cells (MeSH)</term>
<term>Cytotoxicity, Immunologic (MeSH)</term>
<term>Enterotoxins (immunology)</term>
<term>Humans (MeSH)</term>
<term>Immunity, Cellular (MeSH)</term>
<term>In Vitro Techniques (MeSH)</term>
<term>Lymphocyte Activation (MeSH)</term>
<term>Lymphocyte Cooperation (MeSH)</term>
<term>Receptors, Antigen, T-Cell, alpha-beta (immunology)</term>
<term>Receptors, Antigen, T-Cell, gamma-delta (immunology)</term>
<term>Staphylococcus aureus (immunology)</term>
<term>T-Lymphocyte Subsets (immunology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation des lymphocytes (MeSH)</term>
<term>Antigènes bactériens (immunologie)</term>
<term>Clones cellulaires (MeSH)</term>
<term>Coopération des lymphocytes (MeSH)</term>
<term>Cytotoxicité immunologique (MeSH)</term>
<term>Entérotoxines (immunologie)</term>
<term>Humains (MeSH)</term>
<term>Immunité cellulaire (MeSH)</term>
<term>Récepteur lymphocytaire T antigène, alpha-bêta (immunologie)</term>
<term>Récepteur lymphocytaire T antigène, gamma-delta (immunologie)</term>
<term>Sous-populations de lymphocytes T (immunologie)</term>
<term>Staphylococcus aureus (immunologie)</term>
<term>Techniques in vitro (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antigens, Bacterial</term>
<term>Enterotoxins</term>
<term>Receptors, Antigen, T-Cell, alpha-beta</term>
<term>Receptors, Antigen, T-Cell, gamma-delta</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Antigènes bactériens</term>
<term>Entérotoxines</term>
<term>Récepteur lymphocytaire T antigène, alpha-bêta</term>
<term>Récepteur lymphocytaire T antigène, gamma-delta</term>
<term>Sous-populations de lymphocytes T</term>
<term>Staphylococcus aureus</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Staphylococcus aureus</term>
<term>T-Lymphocyte Subsets</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Clone Cells</term>
<term>Cytotoxicity, Immunologic</term>
<term>Humans</term>
<term>Immunity, Cellular</term>
<term>In Vitro Techniques</term>
<term>Lymphocyte Activation</term>
<term>Lymphocyte Cooperation</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation des lymphocytes</term>
<term>Clones cellulaires</term>
<term>Coopération des lymphocytes</term>
<term>Cytotoxicité immunologique</term>
<term>Humains</term>
<term>Immunité cellulaire</term>
<term>Techniques in vitro</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Staphylococcal enterotoxins (SE) are known to stimulate a large proportion of T cells. SE bind to MHC-class II molecules on APC and a particular segment of certain TCR V beta and V gamma gene products. Resting human T cells do not express HLA class II Ag and therefore cannot present SE to T cells. Activated human T cells, however, do express HLA-DR, -DP, and -DQ Ag and could consequently serve as APC for SE. As such, local immune responses to SE might be regulated and/or abrogated by SE-mediated T-T cell interactions leading to T cell destruction. We have investigated if such SE-mediated T-T cell interactions can occur in vitro using human cytolytic TCR-alpha beta+ and TCR-gamma delta+ T cell clones. We demonstrate that the TCR-alpha beta+ T cell clones can efficiently present staphylococcal enterotoxin A (SEA) to each other: T cell clones coated with SEA are lysed by SEA-reactive T cell clones but not by a SEA-nonreactive T cell clone. Furthermore, the SEA-reactive TCR-alpha beta+ clones (but not the SEA-nonreactive clone) destruct themselves in the presence of SEA at low concentrations of SEA (less than 0.01 microgram/ml). Also, SEA-coated T cell clones can induce proliferative responses although such responses are much weaker than those induced when B cells are used as stimulator cells. In contrast, the SEA-reactive TCR-gamma delta+ T cell clones are resistant to autokilling in the presence of SEA and they do not lyse SEA-coated TCR-gamma delta+ targets. However, such targets can be lysed by TCR-alpha beta+ effector cells. These results indicate that TCR-gamma delta+ cells are relatively resistant to lysis and that during local nonspecific immune responses triggered by SE, which induces HLA-class II expression by the responding T cells, SE-mediated T-T cell interactions may play a role in the regulation and/or abrogation of these immune responses.</div>
</front>
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<DateRevised><Year>2014</Year>
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<Title>Journal of immunology (Baltimore, Md. : 1950)</Title>
<ISOAbbreviation>J Immunol</ISOAbbreviation>
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<ArticleTitle>Staphylococcal enterotoxin-mediated human T-T cell interactions.</ArticleTitle>
<Pagination><MedlinePgn>317-22</MedlinePgn>
</Pagination>
<Abstract><AbstractText>Staphylococcal enterotoxins (SE) are known to stimulate a large proportion of T cells. SE bind to MHC-class II molecules on APC and a particular segment of certain TCR V beta and V gamma gene products. Resting human T cells do not express HLA class II Ag and therefore cannot present SE to T cells. Activated human T cells, however, do express HLA-DR, -DP, and -DQ Ag and could consequently serve as APC for SE. As such, local immune responses to SE might be regulated and/or abrogated by SE-mediated T-T cell interactions leading to T cell destruction. We have investigated if such SE-mediated T-T cell interactions can occur in vitro using human cytolytic TCR-alpha beta+ and TCR-gamma delta+ T cell clones. We demonstrate that the TCR-alpha beta+ T cell clones can efficiently present staphylococcal enterotoxin A (SEA) to each other: T cell clones coated with SEA are lysed by SEA-reactive T cell clones but not by a SEA-nonreactive T cell clone. Furthermore, the SEA-reactive TCR-alpha beta+ clones (but not the SEA-nonreactive clone) destruct themselves in the presence of SEA at low concentrations of SEA (less than 0.01 microgram/ml). Also, SEA-coated T cell clones can induce proliferative responses although such responses are much weaker than those induced when B cells are used as stimulator cells. In contrast, the SEA-reactive TCR-gamma delta+ T cell clones are resistant to autokilling in the presence of SEA and they do not lyse SEA-coated TCR-gamma delta+ targets. However, such targets can be lysed by TCR-alpha beta+ effector cells. These results indicate that TCR-gamma delta+ cells are relatively resistant to lysis and that during local nonspecific immune responses triggered by SE, which induces HLA-class II expression by the responding T cells, SE-mediated T-T cell interactions may play a role in the regulation and/or abrogation of these immune responses.</AbstractText>
</Abstract>
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