Partial activation of CD8+ T cells by a self-derived peptide
Identifieur interne : 001D07 ( Main/Exploration ); précédent : 001D06; suivant : 001D08Partial activation of CD8+ T cells by a self-derived peptide
Auteurs : Wuxiong Cao ; Scott S. Tykodi ; Mark T. Esser ; Vivian L. Braciale ; Thomas J. BracialeSource :
- Nature [ 0028-0836 ] ; 1995-11-16.
Abstract
T CELLS are normally activated when the peptide for which they are specific is presented to them in the context of the appropriate major histocompatibility complex (MHC) (class I and Class II for CD8+ and CD4+ T cells, respectively). An increasing body of evidence indicates that structural homologues of the immunogenic peptide can partially activate or antagonize CD4+ T cells13. CD8+ T cells may also be partially antagonized by such peptides4,5, and self-derived peptides of thistype may play a role in CD8+ T cell selection in the thymus68. Activated CD8+ T cells lyse their targets by perforin-dependent granule exocytosis9,10 and by inducing apoptosis mediated by CD95 (also known as Fas or APO1) with its ligand (CD95L)1115. Here we show that a clone of Kd-restricted CD8+ T cells specific for influenza haemagglutinin, which can also be activated in a crossreactive manner by a peptide derived from a myeloma tumour immunoglobulin heavy-chain variableregion (IgVH) to kill by both routes16, kills only by the CD95-CD95L pathway when stimulated by the corresponding germline IgVH peptide. As this germline IgVH peptide differs from the tumour peptide only at a single position buried in the MHC-binding groove, this indicates that CD95CD95L-mediated killing can be triggered independently of the perforin-mediated pathway, and can be selectively affected by changes in MHC conformation.
Url:
DOI: 10.1038/378295a0
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Tykodi</name></author><author><name sortKey="Esser, Mark T" sort="Esser, Mark T" uniqKey="Esser M" first="Mark T." last="Esser">Mark T. Esser</name></author><author><name sortKey="Braciale, Vivian L" sort="Braciale, Vivian L" uniqKey="Braciale V" first="Vivian L." last="Braciale">Vivian L. Braciale</name></author><author><name sortKey="Braciale, Thomas J" sort="Braciale, Thomas J" uniqKey="Braciale T" first="Thomas J." last="Braciale">Thomas J. Braciale</name></author></analytic><monogr></monogr><series><title level="j" type="main">Nature</title><imprint><publisher>Nature Publishing Group</publisher><date when="1995-11-16">1995-11-16</date><biblScope unit="vol">378</biblScope><biblScope unit="issue">6554</biblScope><biblScope unit="page" from="295">295</biblScope><biblScope unit="page" to="298">298</biblScope><date type="Copyright" when="1995">1995</date></imprint><idno type="ISSN">0028-0836</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0028-0836</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">T CELLS are normally activated when the peptide for which they are specific is presented to them in the context of the appropriate major histocompatibility complex (MHC) (class I and Class II for CD8+ and CD4+ T cells, respectively). An increasing body of evidence indicates that structural homologues of the immunogenic peptide can partially activate or antagonize CD4+ T cells13. CD8+ T cells may also be partially antagonized by such peptides4,5, and self-derived peptides of thistype may play a role in CD8+ T cell selection in the thymus68. Activated CD8+ T cells lyse their targets by perforin-dependent granule exocytosis9,10 and by inducing apoptosis mediated by CD95 (also known as Fas or APO1) with its ligand (CD95L)1115. Here we show that a clone of Kd-restricted CD8+ T cells specific for influenza haemagglutinin, which can also be activated in a crossreactive manner by a peptide derived from a myeloma tumour immunoglobulin heavy-chain variableregion (IgVH) to kill by both routes16, kills only by the CD95-CD95L pathway when stimulated by the corresponding germline IgVH peptide. As this germline IgVH peptide differs from the tumour peptide only at a single position buried in the MHC-binding groove, this indicates that CD95CD95L-mediated killing can be triggered independently of the perforin-mediated pathway, and can be selectively affected by changes in MHC conformation.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Braciale, Thomas J" sort="Braciale, Thomas J" uniqKey="Braciale T" first="Thomas J." last="Braciale">Thomas J. Braciale</name><name sortKey="Braciale, Vivian L" sort="Braciale, Vivian L" uniqKey="Braciale V" first="Vivian L." last="Braciale">Vivian L. Braciale</name><name sortKey="Cao, Wuxiong" sort="Cao, Wuxiong" uniqKey="Cao W" first="Wuxiong" last="Cao">Wuxiong Cao</name><name sortKey="Esser, Mark T" sort="Esser, Mark T" uniqKey="Esser M" first="Mark T." last="Esser">Mark T. Esser</name><name sortKey="Tykodi, Scott S" sort="Tykodi, Scott S" uniqKey="Tykodi S" first="Scott S." last="Tykodi">Scott S. 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