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<p>CD4+ T cells are crucial for protective immunity to intracellular pathogens. In addition to secreting cytokines, CD4+ T cells promote control of <i>Mycobacterium tuberculosis</i> 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, <i>Slamf1</i><sup><i>−/−</i></sup> mice have higher Mtb burden and more rapid disease progression than wild type mice. Using <i>Slamf1</i><sup><i>fl/fl</i></sup> conditional knock-out mice, we show that in vivo <i>Slamf1</i> 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月23日

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  • 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,
  • Jennifer A. Philips

摘要

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.