CCL17 high-expression was significantly positively associated with age and advanced N classification, suggesting that CCL17 could accelerate tumor progression by promoting the lymph node metastasis. CCL17 high-expression in THCA tumor microenvironment (TME) accelerates local infiltration of immune cells and enhances anticancer immunity, resulting in worse survival of patients and exerting potential prognostic value on tumor immunity in THCA.

In conclusion, our data demonstrate that sterile pyramidal neuronal death is sufficient to cause epilepsy in the absence of other pathological processes. The CCL17-DTR mouse line may thus be a valuable model for further mechanistic studies on epilepsy and assessment of antiseizure medication.

To conclude, M2-like macrophages-derived CCL17 could facilitate ESCC cell migration and invasion and enhance stemness characteristics of ESCC cells via activating CCR4/ERK/PD-L1 signaling.

In this regard, we present a review on the expression and role of the CCL17/CCL22-CCR4 axis in HM, including lymphoma, leukemia, and multiple myeloma, with the aim of providing latest ideas and directions for the diagnosis and treatment of HM. In addition, we discuss the role and related mechanisms of HM therapeutic agents targeting the CCL17/CCL22-CCR4 axis and the potential of humanized anti-CCR4 antibodies for the treatment of HM.

The mRNA expression level of CCR4 was increased in NDMM patients with combined anemia and renal damage (all P<0.05) . CCL17, CCL22, and CCR4 were highly expressed in clinical samples from patients with NDMM compared to those from controls, and they may be involved in the occurrence and development of NDMM.

The CCL17/CCL22-CCR4 axis can be used as a novel predictive and prognostic biomarker in B-ALL.

These data indicate that T-LBL patients with a NOTCH1 fusion have a high risk of relapse which can be easily identified using a blood CCL17 screening at diagnosis. Further molecular characterization through NOTCH1 gene fusion analysis offers these patients the opportunity for treatment intensification or new treatment strategies.

This comprehensive evaluation of CCR4, CCL17, and associated markers introduces a nuanced understanding of the HCC immunological milieu, proposing CCR4 + CD73 + stromal cells as critical to HCC pathogenesis and patient stratification.

We provided direct evidence of antitumor functions of CCL17 mediated by the recruitment of conventional T cells, NKT cells, and NK cells. Clinical survival outcomes of target gene (CCL17, CCL22, and CCR4) expression also identified that CCL17/CCL22-CCR4 axis is not a marker of poor prognosis.

P=N/A, N=32, Completed, Centre for Human Drug Research, Netherlands | Recruiting --> Completed

TCGA analysis identified that CXCL17 was negatively correlated with some cancer-promoting pathways and involved in inflammatory activities. CTRP analysis revealed that gastric cell lines expressing less CXCL17 and were more sensitive to the CXCR2 inhibitor SB-225002.