iScience · 2026
A specialized CD107a+ macrophage subset drives hyperphagocytosis of mycobacteria.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Eto Carolina, Luiz Gabriela, Silva Hernandez M, Munari Eduarda L, Mendes Daniel A G B, Beck Bianca K, Mascarin Lucas Z, Starick Marick, Canesso Maria Cecília C, Reis Bernardo S, Silveira Guilherme, Bordignon Juliano, de Menezes Yonne K T, Mansur Daniel S, da Rocha Edroaldo Lummertz, Báfica André Luiz Barbosa
Аннотация
Macrophages are essential for pathogen clearance, yet phagocytic specialization among subsets is poorly defined. Bone marrow-derived macrophages cultured with L929 supernatant or macrophage colony-stimulating factor (M-CSF) separate into FSCloSSCloF4/80loCD11blo (FSCloSSClo) and FSChiSSChiF4/80hiCD11bhi (FSChiSSChi) subsets. Transcriptomic and functional analyses reveal that FSCloSSClo cells possess a hyperphagocytic program driven by enhanced actin cytoskeleton regulators (e.g., Arp2/3) and pro-inflammatory signaling (NF-κB). These cells excel at internalizing Mycobacterium tuberculosis virulent H37Rv and BCG through actin-mediated, cytochalasin D-sensitive mechanisms. High surface CD107a (LAMP1) expression marks this hyperphagocytic subset and correlates strongly with mycobacterial uptake. FSCloSSClo macrophages produce more TNF and IL-6 upon mycobacterial or Toll-like receptor 2 (TLR2)/TLR5 stimulation yet retain IFN-γ-mediated killing capacity. In vivo, CD107a+ alveolar macrophages in BCG-infected lungs preferentially capture bacilli and upregulate CD195, recapitulating the in vitro phenotype. These findings establish CD107a as a key surface marker of a hyperphagocytic macrophage subset, providing new mechanistic understanding relevant to tuberculosis host defense and therapeutic development.