IMEX   05356
INSTITUTO DE MEDICINA EXPERIMENTAL
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Impaired CD16+ monocytes differentiation into dendritic cells is mediated by p38-mapk in tuberculosis
Autor/es:
BALBOA L; ROMERO MM; LABORDE E; MUSELLA MR; SASIAIN MC; ALEMÁN M
Lugar:
Lima
Reunión:
Congreso; INMUNOPERÚ 2012; 2012
Institución organizadora:
Asociación Latinoamericana de Inmunología
Resumen:
Background: Tuberculosis (TB) remains as one of the world´s most pernicious diseases mainly due to immune evasion strategies displayed by Mycobacterium tuberculosis (Mtb). Blood monocytes (Mo) represent an important source of dendritic cells (DC) during chronic infections; consequently the alteration of their differentiation constitutes an escape mechanism leading to mycobacterial persistence. We evaluated if the increased CD16+/CD16- Mo ratio displayed by TB patients could explain their impaired differentiation into DC. Methods: Magnetically isolated Mo subsets were differentiated into DC with IL-4 and GM-CSF, and their phenotype and ability to stimulate Mtb-specific T-cells were assessed. Results: CD16- Mo differentiated into efficient antigen presenting CD1a+DC-SIGNhigh DC while CD16+ Mo differentiated into poor antigen presenting CD1alowDC-SIGNlow DC. The addition of CD16+ Mo to CD16- Mo prompted an altered DC profile and CD16+-depleted Mo from TB patients gave rise to CD1a+DC-SIGNhigh. Interestingly, CD16+ Mo did not impair the CD16- Mo differentiation. Finally, the differential p38 MAPK activity in Mo subsets modulated their capacity to generate DC. Conclusions: Mo from TB patients are less prone to differentiate in vitro into DC due to their increased proportion of CD16+ Mo suggesting that during Mtb infection, Mo subsets may have different fates after entering lungs.