Discover how CXCL12+ dermal fibroblasts play a crucial role in boosting our body’s defense mechanisms by attracting neutrophils in response to IL-17, a key finding that could revolutionize treatments in dermatology.
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CXCL12+ dermal fibroblasts promote neutrophil recruitment and host defense by recognition of IL-17.
Cavagnero et al., J Exp Med 2024
<!– DOI: 10.1084/jem.20231425 //–>
https://doi.org/10.1084/jem.20231425
This study delves into the intricate communication network between cells in the skin, particularly during an invasive S. aureus infection in mice. Through an unbiased network analysis, the research highlights the significant role of CXCL12+ fibroblast subsets in facilitating neutrophil communication. These fibroblasts, primarily located in the reticular dermis, are characterized by their expression of adipocyte lineage markers and their ability to detect IL-17 and TNFα. They are crucial for neutrophil recruitment, leveraging NFKBIZ-dependent mechanisms to release CXCR2 ligands and CXCL12. The study further demonstrates that deleting Il17ra in mouse fibroblasts significantly hampers neutrophil recruitment, leading to increased S. aureus infection. Interestingly, similar CXCL12+ fibroblast subsets in humans, particularly in psoriatic skin, show a high expression of neutrophil chemotactic factors, which decrease with IL-17 targeted therapy. This research underscores the pivotal role of CXCL12+ dermal fibroblast subsets in skin immunity, offering insights into potential therapeutic targets for enhancing host defense mechanisms.