IMEX   05356
INSTITUTO DE MEDICINA EXPERIMENTAL
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Signaling Lymphocytic Activation Molecule (SLAM): a molecule that counteracts M. tuberculosis macrophages? immune evasion?
Autor/es:
BARBERO, AM.; ESTERMANN, M.; BALBOA, L.; CELANO, J.; GENOULA, M.; PASQUINELLI, V.; HERNÁNDEZ DEL PINO, RE.; TROTTA, A.; BARRIONUEVO, P.
Lugar:
Mar del Plata, Buenos Aires
Reunión:
Congreso; LXVI Reunión Anual de la Sociedad Argentina de Inmunología (SAI); 2018
Institución organizadora:
Sociedad Argentina de Inmunología (SAI)
Resumen:
Far from being an eradicated disease, Tuberculosis is nowadays the leading cause of death from a pathogen worldwide. Mycobacterium tuberculosis (Mtb) has smartly manipulated the immune system to survive within macrophages over ages.The costimulatory molecule SLAM is a self-ligand receptor that can internalize Gram-negative bacteria and regulate macrophages? phagosomal functions. In tuberculosis SLAM promotes Th1 protective responses.Here we studied SLAM modulation during Mtb infection and its role on macrophages? functions.Human monocyte-derived macrophages were obtained from healthy donors by CD14 positive selection. After 2h of adherence, cells were cultured in complete media overnight before stimulation with sonicated Mtb. THP-1 cells differentiated with PMA and stimulated with Mtb were also used. In some experiments macrophages were additionally stimulated with rhIFN-γ, rhIl-4, rhIl-10 or agonistic anti-SLAM antibody.Our results showed that Mtb-induced SLAM expression, determined by flow cytometry, was increased by IFN-Υ and IL-10 treatment. No changes where observed with lL-4. Moreover, IFN-γ increased TNF-α secretion in Mtb-stimulated THP-1 cells as measured by ELISA.Rhodamine-stained Mtb (Mtb-R) was used to study SLAM role on bacterial uptake by flow cytometry. Anti-SLAM treatment further induced Mtb-R phagocytosis (p