Inhibition by chloroquine of the class II major histocompatibility complex-restricted presentation of endogenous antigens varies according to the cellular origin of the antigen-presenting cells, the nature of the T-cell epitope, and the responding T cell.
Identifieur interne : 000434 ( France/Analysis ); précédent : 000433; suivant : 000435Inhibition by chloroquine of the class II major histocompatibility complex-restricted presentation of endogenous antigens varies according to the cellular origin of the antigen-presenting cells, the nature of the T-cell epitope, and the responding T cell.
Auteurs : S. Lombard-Platlet ; P. Bertolino [France] ; H. Deng [République populaire de Chine] ; D. Gerlier [France] ; C. Rabourdin-Combe [France]Source :
- Immunology [ 0019-2805 ] ; 1993-12-01.
Abstract
Chloroquine treatment of antigen-presenting cells (APC) was explored as a tool to investigate the processing pathway for major histocompatibility complex (MHC) class II-restricted presentation of the endogenous secreted hen egg lysozyme (HEL) and transmembrane measles virus haemagglutinin (HA). A 72-hr pretreatment of the APC with 25 microM chloroquine blocked the presentation of the HEL(52-61) T-cell epitope generated from endogenous HEL to the I-Ak-restricted 3A9 T-cell hybridoma by MHC class II-transfected L cells expressing the invariant chain (Ii). The presentation of exogenously added HEL peptides was not affected. Under the same conditions, no inhibition of the presentation of HEL(106-116) to the I-Ed-restricted G28 high-avidity T-cell hybridoma, nor of HA when synthesized by L cells, was observed. When B-lymphoid APC were used, inhibition was observed in every case with a low number of B APC pretreated for 48 hr with chloroquine prior to the T-cell stimulation test. Moreover, addition of chloroquine to untreated B APC during the T-cell stimulation assay was sufficient to inhibit completely the presentation of HEL(106-116) to the B10.D24.42 low avidity T-cell hybridoma. Altogether these studies suggest that an apparent resistance of endogenous Ag presentation to chloroquine inhibition may not necessarily indicate the existence of a non-endosomal pathway but may be due to the nature of the T-cell epitope, to the use of 'non-professional' APC such as L cells, to the use of T cells of high avidity, and to high amounts of pre-existing MHC class II-peptide complexes expressed by the APC. We demonstrate here that, at least in conventional APC such as B cells, class II-restricted presentation of both endogenous secreted HEL and transmembrane HA involves an endosomal pathway.
Url:
Affiliations:
- France, République populaire de Chine
- Auvergne-Rhône-Alpes, Rhône-Alpes
- Lyon
- Université Claude Bernard Lyon 1, Université de Lyon
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Links to Exploration step
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<date type="start">1939-10-19</date>
<desc> <address> <country key="FR"></country>
</address>
<ref type="url">http://www.cnrs.fr/</ref>
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<country>France</country>
<placeName><settlement type="city">Lyon</settlement>
<region type="region" nuts="2">Auvergne-Rhône-Alpes</region>
<region type="old region" nuts="2">Rhône-Alpes</region>
</placeName>
<orgName type="university">Université Claude Bernard Lyon 1</orgName>
<orgName type="institution" wicri:auto="newGroup">Université de Lyon</orgName>
</affiliation>
</author>
<author><name sortKey="Rabourdin Combe, C" sort="Rabourdin Combe, C" uniqKey="Rabourdin Combe C" first="C." last="Rabourdin-Combe">C. Rabourdin-Combe</name>
<affiliation wicri:level="1"><hal:affiliation type="laboratory" xml:id="struct-27478" status="OLD"> <orgName>Immunité infection vaccination</orgName>
<orgName type="acronym">I2V</orgName>
<desc> <address> <addrLine>CERVI 21, avenue tony garnier 69365 LYON CEDEX 07</addrLine>
<country key="FR"></country>
</address>
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<orgName>Université Claude Bernard Lyon 1</orgName>
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<desc> <address> <addrLine>43, boulevard du 11 novembre 1918, 69622 Villeurbanne cedex</addrLine>
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<ref type="url">https://www.universite-lyon.fr/</ref>
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<tutelle name="U851" active="#struct-303623" type="direct"><org type="institution" xml:id="struct-303623" status="VALID"> <idno type="IdRef">026388278</idno>
<orgName>Institut National de la Santé et de la Recherche Médicale</orgName>
<orgName type="acronym">INSERM</orgName>
<desc> <address> <addrLine>101, rue de Tolbiac, 75013 Paris </addrLine>
<country key="FR"></country>
</address>
<ref type="url">http://www.inserm.fr</ref>
</desc>
</org>
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</hal:affiliation>
<country>France</country>
<placeName><settlement type="city">Lyon</settlement>
<region type="region" nuts="2">Auvergne-Rhône-Alpes</region>
<region type="old region" nuts="2">Rhône-Alpes</region>
</placeName>
<orgName type="university">Université Claude Bernard Lyon 1</orgName>
<orgName type="institution" wicri:auto="newGroup">Université de Lyon</orgName>
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<series><title level="j">Immunology</title>
<idno type="ISSN">0019-2805</idno>
<imprint><date type="datePub">1993-12-01</date>
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<front><div type="abstract" xml:lang="en"> <p>Chloroquine treatment of antigen-presenting cells (APC) was explored as a tool to investigate the processing pathway for major histocompatibility complex (MHC) class II-restricted presentation of the endogenous secreted hen egg lysozyme (HEL) and transmembrane measles virus haemagglutinin (HA). A 72-hr pretreatment of the APC with 25 microM chloroquine blocked the presentation of the HEL(52-61) T-cell epitope generated from endogenous HEL to the I-Ak-restricted 3A9 T-cell hybridoma by MHC class II-transfected L cells expressing the invariant chain (Ii). The presentation of exogenously added HEL peptides was not affected. Under the same conditions, no inhibition of the presentation of HEL(106-116) to the I-Ed-restricted G28 high-avidity T-cell hybridoma, nor of HA when synthesized by L cells, was observed. When B-lymphoid APC were used, inhibition was observed in every case with a low number of B APC pretreated for 48 hr with chloroquine prior to the T-cell stimulation test. Moreover, addition of chloroquine to untreated B APC during the T-cell stimulation assay was sufficient to inhibit completely the presentation of HEL(106-116) to the B10.D24.42 low avidity T-cell hybridoma. Altogether these studies suggest that an apparent resistance of endogenous Ag presentation to chloroquine inhibition may not necessarily indicate the existence of a non-endosomal pathway but may be due to the nature of the T-cell epitope, to the use of 'non-professional' APC such as L cells, to the use of T cells of high avidity, and to high amounts of pre-existing MHC class II-peptide complexes expressed by the APC. We demonstrate here that, at least in conventional APC such as B cells, class II-restricted presentation of both endogenous secreted HEL and transmembrane HA involves an endosomal pathway.</p>
</div>
</front>
</TEI>
<affiliations><list><country><li>France</li>
<li>République populaire de Chine</li>
</country>
<region><li>Auvergne-Rhône-Alpes</li>
<li>Rhône-Alpes</li>
</region>
<settlement><li>Lyon</li>
</settlement>
<orgName><li>Université Claude Bernard Lyon 1</li>
<li>Université de Lyon</li>
</orgName>
</list>
<tree><noCountry><name sortKey="Lombard Platlet, S" sort="Lombard Platlet, S" uniqKey="Lombard Platlet S" first="S" last="Lombard-Platlet">S. Lombard-Platlet</name>
</noCountry>
<country name="France"><region name="Auvergne-Rhône-Alpes"><name sortKey="Bertolino, P" sort="Bertolino, P" uniqKey="Bertolino P" first="P." last="Bertolino">P. Bertolino</name>
</region>
<name sortKey="Gerlier, D" sort="Gerlier, D" uniqKey="Gerlier D" first="D." last="Gerlier">D. Gerlier</name>
<name sortKey="Rabourdin Combe, C" sort="Rabourdin Combe, C" uniqKey="Rabourdin Combe C" first="C." last="Rabourdin-Combe">C. Rabourdin-Combe</name>
</country>
<country name="République populaire de Chine"><noRegion><name sortKey="Deng, H" sort="Deng, H" uniqKey="Deng H" first="H." last="Deng">H. Deng</name>
</noRegion>
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