Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells

Autores
del Balzo, Diego Damián; Capmany, Anahi; Cebrián, José Ignacio; Damiani, María Teresa
Año de publicación
2020
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Chlamydia trachomatis (CT) is an obligate intracellular pathogen and the leading bacterial sexually transmitted infection worldwide. Inside the cell, CT lives into a parasitophorous vacuole (inclusion). Recently DC has begun to be studied like a CT host. Dendritic cells (DCs) can cross-present exogenous antigens to T CD8+ lymphocytes, a process that requires several intracellular transport pathways. Knowing that CT perturbs the intracellular transport, we hypothesized that chlamydia may alter antigen cross-presentation by disturbing key intracellular transport events. By using the DC line JAWS-II and the CT serovar L2, wee observed that CT evades most of the interaction with the endocytic pathway since CT does not localize to specific markers of early endosomes, lysosomes or multivesicular bodies. However, CT did showed a strong interaction with the recycling pathway marker TfR or with different Rab proteins that control endocytic recycling. . Also by confocal microscopy we evidenced a striking redistribution of MHC-I molecules in CT infected DCs. These cells lost their typical MHC-I location in both, the perinuclear recycling center and the plasma membrane. By flow cytometry and WB analysis, we confirmed that MHC-I molecules do not transport properly to the cell surface in infected DCs, as compared to uninfected cells. Although the total amounts of MHC-I molecules are similar in both conditions. . By using the model antigen ovalbumin (OVA) and the specific CD8+ T lymphocytes (B3Z) to measure cross-presentation, we found a significant decrease in the cross-presentation ability of infected DCs with both, soluble and latex beads-associated OVA. Finally, we discarded that this effect is caused by loss of endocytic capacity in the infected DC, since the endocytosis rate remained unchanged after chlamydia infection. Altogether these results indicate that CT infection alters the normal MHC-I intracellular distribution and impairs antigen cross-presentation by DCs.
Fil: del Balzo, Diego Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
Fil: Capmany, Anahi. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
Fil: Cebrián, José Ignacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina
Fil: Damiani, María Teresa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina
LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de Ia Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología
Buenos Aires
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Sociedad Argentina De Fisiología
Materia
CHLAMYDIA TRACHOMATIS
CROSS-PRESENTATION
MHC-I
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/199248
Acceder
id CONICETDig_d6e715c908eefabd52687b58ea8877e3
oai_identifier_str oai:ri.conicet.gov.ar:11336/199248
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cellsdel Balzo, Diego DamiánCapmany, AnahiCebrián, José IgnacioDamiani, María TeresaCHLAMYDIA TRACHOMATISCROSS-PRESENTATIONMHC-Ihttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Chlamydia trachomatis (CT) is an obligate intracellular pathogen and the leading bacterial sexually transmitted infection worldwide. Inside the cell, CT lives into a parasitophorous vacuole (inclusion). Recently DC has begun to be studied like a CT host. Dendritic cells (DCs) can cross-present exogenous antigens to T CD8+ lymphocytes, a process that requires several intracellular transport pathways. Knowing that CT perturbs the intracellular transport, we hypothesized that chlamydia may alter antigen cross-presentation by disturbing key intracellular transport events. By using the DC line JAWS-II and the CT serovar L2, wee observed that CT evades most of the interaction with the endocytic pathway since CT does not localize to specific markers of early endosomes, lysosomes or multivesicular bodies. However, CT did showed a strong interaction with the recycling pathway marker TfR or with different Rab proteins that control endocytic recycling. . Also by confocal microscopy we evidenced a striking redistribution of MHC-I molecules in CT infected DCs. These cells lost their typical MHC-I location in both, the perinuclear recycling center and the plasma membrane. By flow cytometry and WB analysis, we confirmed that MHC-I molecules do not transport properly to the cell surface in infected DCs, as compared to uninfected cells. Although the total amounts of MHC-I molecules are similar in both conditions. . By using the model antigen ovalbumin (OVA) and the specific CD8+ T lymphocytes (B3Z) to measure cross-presentation, we found a significant decrease in the cross-presentation ability of infected DCs with both, soluble and latex beads-associated OVA. Finally, we discarded that this effect is caused by loss of endocytic capacity in the infected DC, since the endocytosis rate remained unchanged after chlamydia infection. Altogether these results indicate that CT infection alters the normal MHC-I intracellular distribution and impairs antigen cross-presentation by DCs.Fil: del Balzo, Diego Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Capmany, Anahi. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Cebrián, José Ignacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaFil: Damiani, María Teresa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; ArgentinaLXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de Ia Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de FisiologíaBuenos AiresArgentinaSociedad Argentina de Investigación ClínicaSociedad Argentina de InmunologíaSociedad Argentina De FisiologíaFundación Revista Medicina2020info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/199248Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de Ia Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Buenos Aires; Argentina; 2020; 167-1670025-7680CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://inmunologia.org.ar/reunion-anual-de-sociedades-de-biociencia-2020/Nacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:39:02Zoai:ri.conicet.gov.ar:11336/199248instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-15 15:39:03.23CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells
title Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells
spellingShingle Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells
del Balzo, Diego Damián
CHLAMYDIA TRACHOMATIS
CROSS-PRESENTATION
MHC-I
title_short Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells
title_full Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells
title_fullStr Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells
title_full_unstemmed Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells
title_sort Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells
dc.creator.none.fl_str_mv del Balzo, Diego Damián
Capmany, Anahi
Cebrián, José Ignacio
Damiani, María Teresa
author del Balzo, Diego Damián
author_facet del Balzo, Diego Damián
Capmany, Anahi
Cebrián, José Ignacio
Damiani, María Teresa
author_role author
author2 Capmany, Anahi
Cebrián, José Ignacio
Damiani, María Teresa
author2_role author
author
author
dc.subject.none.fl_str_mv CHLAMYDIA TRACHOMATIS
CROSS-PRESENTATION
MHC-I
topic CHLAMYDIA TRACHOMATIS
CROSS-PRESENTATION
MHC-I
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Chlamydia trachomatis (CT) is an obligate intracellular pathogen and the leading bacterial sexually transmitted infection worldwide. Inside the cell, CT lives into a parasitophorous vacuole (inclusion). Recently DC has begun to be studied like a CT host. Dendritic cells (DCs) can cross-present exogenous antigens to T CD8+ lymphocytes, a process that requires several intracellular transport pathways. Knowing that CT perturbs the intracellular transport, we hypothesized that chlamydia may alter antigen cross-presentation by disturbing key intracellular transport events. By using the DC line JAWS-II and the CT serovar L2, wee observed that CT evades most of the interaction with the endocytic pathway since CT does not localize to specific markers of early endosomes, lysosomes or multivesicular bodies. However, CT did showed a strong interaction with the recycling pathway marker TfR or with different Rab proteins that control endocytic recycling. . Also by confocal microscopy we evidenced a striking redistribution of MHC-I molecules in CT infected DCs. These cells lost their typical MHC-I location in both, the perinuclear recycling center and the plasma membrane. By flow cytometry and WB analysis, we confirmed that MHC-I molecules do not transport properly to the cell surface in infected DCs, as compared to uninfected cells. Although the total amounts of MHC-I molecules are similar in both conditions. . By using the model antigen ovalbumin (OVA) and the specific CD8+ T lymphocytes (B3Z) to measure cross-presentation, we found a significant decrease in the cross-presentation ability of infected DCs with both, soluble and latex beads-associated OVA. Finally, we discarded that this effect is caused by loss of endocytic capacity in the infected DC, since the endocytosis rate remained unchanged after chlamydia infection. Altogether these results indicate that CT infection alters the normal MHC-I intracellular distribution and impairs antigen cross-presentation by DCs.
Fil: del Balzo, Diego Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
Fil: Capmany, Anahi. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
Fil: Cebrián, José Ignacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina
Fil: Damiani, María Teresa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina
LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de Ia Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología
Buenos Aires
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Sociedad Argentina De Fisiología
description Chlamydia trachomatis (CT) is an obligate intracellular pathogen and the leading bacterial sexually transmitted infection worldwide. Inside the cell, CT lives into a parasitophorous vacuole (inclusion). Recently DC has begun to be studied like a CT host. Dendritic cells (DCs) can cross-present exogenous antigens to T CD8+ lymphocytes, a process that requires several intracellular transport pathways. Knowing that CT perturbs the intracellular transport, we hypothesized that chlamydia may alter antigen cross-presentation by disturbing key intracellular transport events. By using the DC line JAWS-II and the CT serovar L2, wee observed that CT evades most of the interaction with the endocytic pathway since CT does not localize to specific markers of early endosomes, lysosomes or multivesicular bodies. However, CT did showed a strong interaction with the recycling pathway marker TfR or with different Rab proteins that control endocytic recycling. . Also by confocal microscopy we evidenced a striking redistribution of MHC-I molecules in CT infected DCs. These cells lost their typical MHC-I location in both, the perinuclear recycling center and the plasma membrane. By flow cytometry and WB analysis, we confirmed that MHC-I molecules do not transport properly to the cell surface in infected DCs, as compared to uninfected cells. Although the total amounts of MHC-I molecules are similar in both conditions. . By using the model antigen ovalbumin (OVA) and the specific CD8+ T lymphocytes (B3Z) to measure cross-presentation, we found a significant decrease in the cross-presentation ability of infected DCs with both, soluble and latex beads-associated OVA. Finally, we discarded that this effect is caused by loss of endocytic capacity in the infected DC, since the endocytosis rate remained unchanged after chlamydia infection. Altogether these results indicate that CT infection alters the normal MHC-I intracellular distribution and impairs antigen cross-presentation by DCs.
publishDate 2020
dc.date.none.fl_str_mv 2020
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
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status_str publishedVersion
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dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/199248
Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de Ia Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Buenos Aires; Argentina; 2020; 167-167
0025-7680
CONICET Digital
CONICET
url http://hdl.handle.net/11336/199248
identifier_str_mv Chlamydia trachomatis disturbs antigen cross-presentation by infected dendritic cells; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVIII Reunión Anual de Ia Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Buenos Aires; Argentina; 2020; 167-167
0025-7680
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
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dc.coverage.none.fl_str_mv Nacional
dc.publisher.none.fl_str_mv Fundación Revista Medicina
publisher.none.fl_str_mv Fundación Revista Medicina
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repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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