dc.creator | Basile, Juan Ignacio | |
dc.creator | Geffner, Laura | |
dc.creator | Romero, María Mercedes | |
dc.creator | Balboa, Luciana | |
dc.creator | Sabio y García, Carmen Alejandra | |
dc.creator | Ritacco, Viviana | |
dc.creator | García, Ana | |
dc.creator | Cuffré, Mónica | |
dc.creator | Abbate, Eduardo | |
dc.creator | López, Beatriz | |
dc.creator | Barrera, Lucía | |
dc.creator | Ambroggi, Marta | |
dc.creator | Alemán, Mercedes | |
dc.creator | Sasiain, María C. | |
dc.creator | de la Barrera, Silvia | |
dc.date | 2021-01-22T19:31:27Z | |
dc.date | 2021-01-22T19:31:27Z | |
dc.date | 2011-10-01 | |
dc.date.accessioned | 2023-08-29T20:09:06Z | |
dc.date.available | 2023-08-29T20:09:06Z | |
dc.identifier | 1537-6613 | |
dc.identifier | http://sgc.anlis.gob.ar/handle/123456789/2237 | |
dc.identifier | 10.1093/infdis/jir460 | |
dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/8520513 | |
dc.description | Fil: Basile, Juan I. Academia Nacional de Medicina. Instituto de Investigaciones Hematológicas Mariano R. Castex; Argentina. | |
dc.description | Fil: Geffner, Laura J. Academia Nacional de Medicina. Instituto de Investigaciones Hematológicas Mariano R. Castex; Argentina. | |
dc.description | Fil: Romero, María M. Academia Nacional de Medicina. Instituto de Investigaciones Hematológicas Mariano R. Castex; Argentina. | |
dc.description | Fil: Balboa, Luciana. Academia Nacional de Medicina. Instituto de Investigaciones Hematológicas Mariano R. Castex; Argentina. | |
dc.description | Fil: Sabio y García, Carmen. Academia Nacional de Medicina. Instituto de Investigaciones Hematológicas Mariano R. Castex; Argentina. | |
dc.description | Fil: Ritacco, Viviana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina. | |
dc.description | Fil: García, Ana. Hospital Muñíz. Instituto de Tisioneumonologías; Argentina. | |
dc.description | Fil: Cuffré, Mónica. Hospital Muñíz. Instituto de Tisioneumonologías; Argentina. | |
dc.description | Fil: Abbate, Eduardo. Hospital Muñíz. Instituto de Tisioneumonologías; Argentina. | |
dc.description | Fil: López, Beatriz. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina. | |
dc.description | Fil: Barrera, Lucía. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina. | |
dc.description | Fil: Ambroggi, Marta. Hospital Muñíz. Instituto de Tisioneumonologías; Argentina. | |
dc.description | Fil: Alemán, Mercedes. Academia Nacional de Medicina. Instituto de Investigaciones Hematológicas Mariano R. Castex; Argentina. | |
dc.description | Fil: Sasiain, María C. Academia Nacional de Medicina. Instituto de Investigaciones Hematológicas Mariano R. Castex; Argentina. | |
dc.description | Fil: de la Barrera, Silvia S. Academia Nacional de Medicina. Instituto de Investigaciones Hematológicas Mariano R. Castex; Argentina. | |
dc.description | Background. The proinflammatory cytokine interleukin 17 (IL-17) plays an important role in immune responses
but it is also associated with tissue-damaging inflammation. So, we evaluated the ability of Mycobacterium tuberculosis
clinical isolates to induce IL-17 in tuberculosis (TB) patients and in healthy human tuberculin reactors (PPD1HD).
Methods. IL-17, interferon c (IFN-c), and interleukin 23 (IL-23) receptor expression were evaluated ex vivo
and cultured peripheral blood mononuclear cells from TB and PPD1HD stimulated with irradiated clinical isolates
from multidrug resistant (MDR) outbreaks M (Haarlem family) and Ra (Latin American–Mediterranean family), as
well as drug-susceptible isolates belonging to the same families and laboratory strain H37Rv for 48 hours in T-cell
subsets by flow cytometry.
Results. We observed that: (1) MDR strains M and Ra are stronger IL-17 inducers than drug-susceptible Mtb
strains of the Haarlem and Latin American–Mediterranean families, (2) MDR-TB patients show the highest IL-17
expression that is independent on the strain, (3) IL-17 expression is dependent on CD41 and CD81 T cells
associates with persistently high antigen load.
Conclusions. IL-17–producing T cells could play an immunopathological role in MDR-TB promoting severe
tissue damage, which may be associated with the low effectiveness of the second-line drugs employed in the treatment. | |
dc.format | pdf | |
dc.language | en | |
dc.relation | The Journal of infectious diseases | |
dc.rights | open | |
dc.source | The Journal of Infectious Diseases 2011;204(7):1054-1064 | |
dc.subject | Mycobacterium tuberculosis | |
dc.subject | Tuberculosis | |
dc.subject | Interleucina-17 | |
dc.subject | Linfocitos T | |
dc.title | Outbreaks of mycobacterium tuberculosis MDR strains induce high IL-17 T-cell response in patients with MDR tuberculosis that is closely associated with high antigen load | |
dc.type | Artículo | |