ArticleFrontiers in immunology2025
Insufficient CXCL13 secretion in leprosy foamy macrophages attenuates lymphocyte recruitment and antimicrobial protein production.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Pathogens trigger metabolic reprogramming, leading to the formation of foamy macrophages (FMs). This process provides a favorable environment for bacterial proliferation and enables bacteria to evade immune killing. Objective: To elucidate the mechanisms by which pathogens escape immune surveillance and elimination via the formation of FMs. Methods: We constructed a FM model using monocyte-derived macrophages (MDMs) that were incubated with oxidized low-density lipoprotein (oxLDL). Subsequently, we employed bulk RNA-sequencing (bulk RNA-seq) to comprehensively analyze the immune responses in MDMs and FMs against Results: We found that CXCL13, a component of the cytokine-cytokine receptor interaction pathway, was specifically upregulated in Conclusion: In conclusion, the NLRP12/NF-κB/CXCL13 axis is crucial for the immune response of FMs after mycobacterial infection. These findings contribute to a deeper understanding of the pathological mechanisms of mycobacterial infection.
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