ArticleCell insight2026
CXCL4 and CXCL4L1 activate human macrophage via TLR4 signaling to modulate inflammatory responses.
Article in Cell insight, 2026. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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18 authors.
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Abstract
The chemokine CXCL4 activates human monocytes/macrophages and contributes to the pathogenesis of inflammatory and fibrotic diseases. However, the receptor of CXCL4, CXCR3, is not expressed in human monocytes/macrophages. Thus, signaling pathways and receptors that mediate human monocytes/macrophages response to CXCL4 alone are not well characterized. Using human primary monocytes and mouse bone marrow-derived macrophages, we reported that CXCL4 activated NF-κB and a TBK1-JNK-AP1 signaling axis that drove the expression of inflammatory, fibrotic and neutrophil chemokine genes, and also a TRIF-RIPK3 axis-dependent necroptosis in primary human monocytes. Surprisingly, multiple evidence targeting TLR4 expression and function suggested a role for TLR4 in CXCL4 responses. Further, we show that CXCL4 and its natural variant CXCL4L1 interact with TLR4/MD-2 complex in human monocytes and CXCL4L1 induced a transcriptomic profile divergent to LPS. Ectopic expression of human CXCL4L1 using adeno-associated virus (AAV) system effectively mitigated papain-induced asthma in wild-type (WT) mice. Notably, the therapeutic impact of CXCL4L1 was absent in
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