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SLAMF1 signaling induces Mycobacterium tuberculosis uptake leading to endolysosomal maturation in human macrophages
Author(s) -
Barbero Angela María,
Trotta Aldana,
Genoula Melanie,
Pino Rodrigo Emanuel Hernández Del,
Estermann Martín Andrés,
Celano Josefina,
Fuentes Federico,
García Verónica Edith,
Balboa Luciana,
Barrionuevo Paula,
Pasquinelli Virginia
Publication year - 2021
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.4ma0820-655rr
Subject(s) - mycobacterium tuberculosis , tuberculosis , biology , endosome , microbiology and biotechnology , macrophage , immunology , medicine , biochemistry , in vitro , intracellular , pathology
Tuberculosis dates back to ancient times but it is not a problem of the past. Each year, millions of people die from tuberculosis. After inhalation of infectious droplet nuclei, Mycobacterium tuberculosis reaches the lungs where it can manipulate the immune system and survive within host macrophages, establishing a persistent infection. The signaling lymphocytic activation molecule family member 1 (SLAMF1) is a self‐ligand receptor that can internalize gram‐negative bacteria and regulate macrophages’ phagosomal functions. In tuberculosis, SLAMF1 promotes Th1‐protective responses. In this work, we studied the role of SLAMF1 on macrophages’ functions during M. tuberculosis infection. Our results showed that both M. tuberculosis and IFN‐γ stimulation induce SLAMF1 expression in macrophages from healthy donor and Tohoku Hospital Pediatrcs‐1 cells. Costimulation through SLAMF1 with an agonistic antibody resulted in an enhanced internalization of M. tuberculosis by macrophages. Interestingly, we found that SLAMF1 interacts with M. tuberculosis and colocalizes with the bacteria and with early and late endosomes/lysosomes markers (EEA1 and LAMP2), suggesting that SLAMF1 recognize M. tuberculosis and participate in the endolysosomal maturation process. Notably, increased levels of SLAMF1 were detected in CD14 cells from pleural effusions of tuberculosis patients, indicating that SLAMF1 might have an active function at the site of infection. Taken together, our results provide evidence that SLAMF1 improves the uptake of M. tuberculosis by human monocyte‐derived macrophages.