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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/199248
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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 Técnicas2025-09-29T10:41:11Zoai: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:34982025-09-29 10:41:11.493CONICET 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 Reunión Journal http://purl.org/coar/resource_type/c_5794 info:ar-repo/semantics/documentoDeConferencia |
status_str |
publishedVersion |
format |
conferenceObject |
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 |
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Fundación Revista Medicina |
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Fundación Revista Medicina |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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