Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulation
- Autores
- Girard, Magalí Celeste; Acevedo, Gonzalo Raúl; Beati, Maria Paula; Fernandez, Marisa; Hernandez, Yolanda; Chadi, Raul; Gomez, Karina Andrea
- Año de publicación
- 2019
- Idioma
- inglés
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- Chronic Chagas disease (CCD) caused by T. cruzi infection is associated with an imbalance between an excessive inflammatory reaction and a defective immunomodulatory profile caused by host-parasite interaction. Despite the growing importance of regulatory B cells in many malignancies, the role of these population remains elusive in CCD. Here, we used flow cytometry to evaluate the phenotype of peripheral blood B cells, isolated from CCD patients with or without cardiac involvement, according to their expression of CD19, CD24, CD38 and CD27. Cells were incubated with or without T. cruzi lysate, and/or CpG and CD40L, and IL-10 production was also assessed by intracellular cytokine staining (ICS). In order to overcome the absence of subset-specific hallmark membrane markers, we performed an automated and nonsupervised analysis method called flowPeaks, based on k-means algorithm for data clustering. flowPeaks identified five clusters according to the simultaneous assessment of the fluorescent markers mentioned above. We found that in T. cruzi-stimulated conditions, CD19highCD27lowCD24low B cells were diminished in CCD patients compared to non-infected donors (p<0.05), while CD19highCD27highCD24high B cells were augmented only in patients with cardiac compromise (p<0.05). Both B cells clusters express variable amounts of CD38. In addition, the proportion of IL-10-producing B cells (B10 cells) was increased in T. cruzi stimulated samples in CCD patients and non-infected donors (p<0.05). Our results suggest that cardiac CCD patients display a memory B cell phenotype upon exposure to T. cruzi, although IL10 production by B cells may be consequence of an innate response triggered by the parasite.
Fil: Girard, Magalí Celeste. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Acevedo, Gonzalo Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Beati, Maria Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
Fil: Fernandez, Marisa. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina
Fil: Hernandez, Yolanda. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina
Fil: Chadi, Raul. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Agudos Doctor Ignacio Pirovano; Argentina
Fil: Gomez, Karina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina
LXVII Reunión Científica Anual de Sociedad Argentina de Inmunología
San Miguel de Tucumán
Argentina
Sociedad Argentina de Inmunologia - Materia
-
TRYPANOSOMA CRUZI
B CELLS
REGULATORY B CELLS
CHAGAS DISEASE - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/275562
Ver los metadatos del registro completo
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Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulationGirard, Magalí CelesteAcevedo, Gonzalo RaúlBeati, Maria PaulaFernandez, MarisaHernandez, YolandaChadi, RaulGomez, Karina AndreaTRYPANOSOMA CRUZIB CELLSREGULATORY B CELLSCHAGAS DISEASEhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Chronic Chagas disease (CCD) caused by T. cruzi infection is associated with an imbalance between an excessive inflammatory reaction and a defective immunomodulatory profile caused by host-parasite interaction. Despite the growing importance of regulatory B cells in many malignancies, the role of these population remains elusive in CCD. Here, we used flow cytometry to evaluate the phenotype of peripheral blood B cells, isolated from CCD patients with or without cardiac involvement, according to their expression of CD19, CD24, CD38 and CD27. Cells were incubated with or without T. cruzi lysate, and/or CpG and CD40L, and IL-10 production was also assessed by intracellular cytokine staining (ICS). In order to overcome the absence of subset-specific hallmark membrane markers, we performed an automated and nonsupervised analysis method called flowPeaks, based on k-means algorithm for data clustering. flowPeaks identified five clusters according to the simultaneous assessment of the fluorescent markers mentioned above. We found that in T. cruzi-stimulated conditions, CD19highCD27lowCD24low B cells were diminished in CCD patients compared to non-infected donors (p<0.05), while CD19highCD27highCD24high B cells were augmented only in patients with cardiac compromise (p<0.05). Both B cells clusters express variable amounts of CD38. In addition, the proportion of IL-10-producing B cells (B10 cells) was increased in T. cruzi stimulated samples in CCD patients and non-infected donors (p<0.05). Our results suggest that cardiac CCD patients display a memory B cell phenotype upon exposure to T. cruzi, although IL10 production by B cells may be consequence of an innate response triggered by the parasite.Fil: Girard, Magalí Celeste. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Acevedo, Gonzalo Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Beati, Maria Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Fernandez, Marisa. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; ArgentinaFil: Hernandez, Yolanda. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; ArgentinaFil: Chadi, Raul. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Agudos Doctor Ignacio Pirovano; ArgentinaFil: Gomez, Karina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaLXVII Reunión Científica Anual de Sociedad Argentina de InmunologíaSan Miguel de TucumánArgentinaSociedad Argentina de InmunologiaSociedad Argentina de Inmunología2019info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónBookhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/275562Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulation; LXVII Reunión Científica Anual de Sociedad Argentina de Inmunología; San Miguel de Tucumán; Argentina; 2019; 63-63978-987-47408-0-9CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://inmunologia.org.ar/lvii-reunion-anual-de-la-sociedad-argentina-de-inmunologia/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 Técnicas2025-12-03T08:56:59Zoai:ri.conicet.gov.ar:11336/275562instacron: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:34982025-12-03 08:57:00.087CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulation |
| title |
Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulation |
| spellingShingle |
Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulation Girard, Magalí Celeste TRYPANOSOMA CRUZI B CELLS REGULATORY B CELLS CHAGAS DISEASE |
| title_short |
Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulation |
| title_full |
Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulation |
| title_fullStr |
Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulation |
| title_full_unstemmed |
Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulation |
| title_sort |
Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulation |
| dc.creator.none.fl_str_mv |
Girard, Magalí Celeste Acevedo, Gonzalo Raúl Beati, Maria Paula Fernandez, Marisa Hernandez, Yolanda Chadi, Raul Gomez, Karina Andrea |
| author |
Girard, Magalí Celeste |
| author_facet |
Girard, Magalí Celeste Acevedo, Gonzalo Raúl Beati, Maria Paula Fernandez, Marisa Hernandez, Yolanda Chadi, Raul Gomez, Karina Andrea |
| author_role |
author |
| author2 |
Acevedo, Gonzalo Raúl Beati, Maria Paula Fernandez, Marisa Hernandez, Yolanda Chadi, Raul Gomez, Karina Andrea |
| author2_role |
author author author author author author |
| dc.subject.none.fl_str_mv |
TRYPANOSOMA CRUZI B CELLS REGULATORY B CELLS CHAGAS DISEASE |
| topic |
TRYPANOSOMA CRUZI B CELLS REGULATORY B CELLS CHAGAS DISEASE |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
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Chronic Chagas disease (CCD) caused by T. cruzi infection is associated with an imbalance between an excessive inflammatory reaction and a defective immunomodulatory profile caused by host-parasite interaction. Despite the growing importance of regulatory B cells in many malignancies, the role of these population remains elusive in CCD. Here, we used flow cytometry to evaluate the phenotype of peripheral blood B cells, isolated from CCD patients with or without cardiac involvement, according to their expression of CD19, CD24, CD38 and CD27. Cells were incubated with or without T. cruzi lysate, and/or CpG and CD40L, and IL-10 production was also assessed by intracellular cytokine staining (ICS). In order to overcome the absence of subset-specific hallmark membrane markers, we performed an automated and nonsupervised analysis method called flowPeaks, based on k-means algorithm for data clustering. flowPeaks identified five clusters according to the simultaneous assessment of the fluorescent markers mentioned above. We found that in T. cruzi-stimulated conditions, CD19highCD27lowCD24low B cells were diminished in CCD patients compared to non-infected donors (p<0.05), while CD19highCD27highCD24high B cells were augmented only in patients with cardiac compromise (p<0.05). Both B cells clusters express variable amounts of CD38. In addition, the proportion of IL-10-producing B cells (B10 cells) was increased in T. cruzi stimulated samples in CCD patients and non-infected donors (p<0.05). Our results suggest that cardiac CCD patients display a memory B cell phenotype upon exposure to T. cruzi, although IL10 production by B cells may be consequence of an innate response triggered by the parasite. Fil: Girard, Magalí Celeste. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina Fil: Acevedo, Gonzalo Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina Fil: Beati, Maria Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina Fil: Fernandez, Marisa. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina Fil: Hernandez, Yolanda. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud “Dr. C. G. Malbrán”. Instituto Nacional de Parasitología "Dr. Mario Fatala Chaben”; Argentina Fil: Chadi, Raul. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Agudos Doctor Ignacio Pirovano; Argentina Fil: Gomez, Karina Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina LXVII Reunión Científica Anual de Sociedad Argentina de Inmunología San Miguel de Tucumán Argentina Sociedad Argentina de Inmunologia |
| description |
Chronic Chagas disease (CCD) caused by T. cruzi infection is associated with an imbalance between an excessive inflammatory reaction and a defective immunomodulatory profile caused by host-parasite interaction. Despite the growing importance of regulatory B cells in many malignancies, the role of these population remains elusive in CCD. Here, we used flow cytometry to evaluate the phenotype of peripheral blood B cells, isolated from CCD patients with or without cardiac involvement, according to their expression of CD19, CD24, CD38 and CD27. Cells were incubated with or without T. cruzi lysate, and/or CpG and CD40L, and IL-10 production was also assessed by intracellular cytokine staining (ICS). In order to overcome the absence of subset-specific hallmark membrane markers, we performed an automated and nonsupervised analysis method called flowPeaks, based on k-means algorithm for data clustering. flowPeaks identified five clusters according to the simultaneous assessment of the fluorescent markers mentioned above. We found that in T. cruzi-stimulated conditions, CD19highCD27lowCD24low B cells were diminished in CCD patients compared to non-infected donors (p<0.05), while CD19highCD27highCD24high B cells were augmented only in patients with cardiac compromise (p<0.05). Both B cells clusters express variable amounts of CD38. In addition, the proportion of IL-10-producing B cells (B10 cells) was increased in T. cruzi stimulated samples in CCD patients and non-infected donors (p<0.05). Our results suggest that cardiac CCD patients display a memory B cell phenotype upon exposure to T. cruzi, although IL10 production by B cells may be consequence of an innate response triggered by the parasite. |
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2019 |
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2019 |
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Regulatory B cells phenotype in patients with chronic Chagas Disease upon T. cruzi stimulation; LXVII Reunión Científica Anual de Sociedad Argentina de Inmunología; San Miguel de Tucumán; Argentina; 2019; 63-63 978-987-47408-0-9 CONICET Digital CONICET |
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