Signaling Lymphocytic Activation Molecule (SLAM): a molecule that counteracts Mycobacterium tuberculosis macrophages' immune evasion?

BARBERO AM; HERNÁNDEZ DEL PINO RE; CELANO J; ESTERMANN MA; TROTTA A; GENOULA M; GARCÍA VE; BALBOA L; BARRIONUEVO P; PASQUINELLI V

Simposio; Keystone Symposia on Molecular and Cellular Biology. Tuberculosis: Mechanisms, Pathogenesis and Treatment; 2019

Far from being an eradicated disease, Tuberculosis (TB) 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 TB SLAM promotes Th1 responses. Here we studied SLAM role on macrophages? functions during Mtb infection. Human monocyte-derived macrophages from healthy donors and THP-1 cells differentiated with PMA were stimulated with sonicated Mtb. Our results showed that Mtb-induced SLAM expression, determined by flow cytometry, was increased by IFN-g and IL-10 treatment. No changes where observed with lL-4. Moreover, IFN-g increased TNF-α secretion in Mtb-stimulated THP-1 cells. Rhodamine-stained Mtb (Mtb-R) was used to study SLAM role on bacterial uptake by flow cytometry. Agonistic anti-SLAM antibody treatment further induced Mtb-R phagocytosis (p