Macrophage-T cell interactions promote SLAMF1 expression for enhanced TB defense

G. V. R. Krishna Prasad, Steven J. Grigsby, Gideon A. Erkenswick, Cynthia Portal-Celhay, Ekansh Mittal, Guozhe Yang, Samuel M. Fallon, Fengyixin Chen, Thais Klevorn, Neharika Jain, Yuanyuan Li, Makedonka Mitreva, Amanda J. Martinot, Joel D. Ernst and Jennifer A. Philips ()
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G. V. R. Krishna Prasad: Department of Medicine; Washington University School of Medicine
Steven J. Grigsby: Department of Medicine; Washington University School of Medicine
Gideon A. Erkenswick: Department of Medicine; Washington University School of Medicine
Cynthia Portal-Celhay: New York University School of Medicine
Ekansh Mittal: Department of Medicine; Washington University School of Medicine
Guozhe Yang: Department of Medicine; Washington University School of Medicine
Samuel M. Fallon: Department of Medicine; Washington University School of Medicine
Fengyixin Chen: Department of Medicine; Washington University School of Medicine
Thais Klevorn: New York University School of Medicine
Neharika Jain: Department of Infectious Disease and Global Health
Yuanyuan Li: Department of Medicine; Washington University School of Medicine
Makedonka Mitreva: Department of Medicine; Washington University School of Medicine
Amanda J. Martinot: Department of Infectious Disease and Global Health
Joel D. Ernst: San Francisco
Jennifer A. Philips: Department of Medicine; Washington University School of Medicine

Nature Communications, 2025, vol. 16, issue 1, 1-17

Abstract: Abstract CD4+ T cells are crucial for protective immunity to intracellular pathogens. In addition to secreting cytokines, CD4+ T cells promote control of Mycobacterium tuberculosis infection through cognate interactions with macrophages, but the mechanism has been unclear. Here, we show that SLAMF1/CD150 is highly and uniquely induced in macrophages by antigen-specific interactions with CD4+ T cells. In macrophages, SLAMF1 enhances the generation of reactive oxygen species and restricts Mtb replication. Mtb-infection of mice promotes SLAMF1 expression specifically on infected macrophages, not uninfected bystanders. SLAMF1 expression depends on adaptive immunity and also autophagy. Moreover, Slamf1−/− mice have higher Mtb burden and more rapid disease progression than wild type mice. Using Slamf1fl/fl conditional knock-out mice, we show that in vivo Slamf1 is specifically required in macrophages to restrict mycobacterial growth and limit IL-1β production. In macaques, macrophage SLAMFI expression also correlates with T cell responses and protection. Combined, these data demonstrate that SLAMF1 is a marker of macrophage-T cells interactions, and it promotes protection against Mtb.

Date: 2025
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DOI: 10.1038/s41467-025-61826-7

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