CCR4 (C-C Motif Chemokine Receptor 4)

Tregs were increased and activated in DTC tumor tissue, indicating that they play an important role in creating an immunosuppressive microenvironment in DTC. The results suggest that eTreg-depletion immunotherapy using an anti-CCR4 antibody (mogamulizumab) might be effective for treating DTC.

When tested in vivo in humanized mice, a single dose of CCR4 CART led to nearly complete Treg depletion. These findings support the potential of CCR4 CARTs as a selective and effective approach to Treg modulation and warrant further clinical investigation.

P1, N=43, Active, not recruiting, UNC Lineberger Comprehensive Cancer Center | Recruiting --> Active, not recruiting | Trial completion date: Sep 2041 --> Nov 2039 | Trial primary completion date: Sep 2026 --> Dec 2025

These findings enhance our understanding of the molecular mechanisms by which BPA induces ccRCC and highlight potential targets for therapeutic intervention, particularly in endocrine and immune-related pathways. This underscores the need for collaborative efforts to mitigate the impact of environmental toxins like BPA on public health.

The present paper provides a comprehensive review of the current literature on the role of the immune system in the inflammatory pain response, with a specific focus on the role of CCL17 and CCL22 activity in the pathophysiology of pain. Also, we discuss the potential for therapeutically targeting CCR4 and its clinical implications.

Additionally, the combination of STL127705, an inhibitor of the XRCC6/XRCC5 heterodimer, with radiotherapy notably suppressed tumor growth in patient-derived xenograft (PDX) and cell line mouse transplant tumor models, especially in the context of CNOT7 deficiency. These findings elucidate the function of CNOT7 in promoting DNA repair and radiotherapy resistance in CRC, highlighting that targeting the CNOT7-TRIM21-XRCC6 axis provides a promising therapeutic approach to overcome radiotherapy resistance and improve clinical outcomes for CRC patients.

Continued refinement through novel designs, such as conditionally activated or bispecific antibodies, will be essential to balance efficacy and safety. Together, these strategies hold potential to establish Treg depletion as a viable therapeutic modality in cancer.

In the cell proliferation assay, chemokine ligands stimulated an increase in EO-1 cells in the WT group, but not in the KO groups. These results suggest that CCR4 or CCR7 plays a vital role in the initial migration to sentinel lymph nodes and proliferation in a canine cutaneous lymphoma model.

This expeditious and simple workflow beginning from docking to compound evaluation identified 3 hits for CCR2 (Ki = 1.3-6 μM) and 1 hit (IC50 = 10.8 μM) for CCR5. The obtained structure-activity relationships were also further rationalized using structural information available for both CCR5 and CCR2 providing valuable insights for future development of intracellular allosteric ligands.

Our study provides novel insights into the molecular properties of residual malignant clones within MAR that appear silenced, surrounded by a putatively anti-tumor immune response.

Therefore, this review summarizes recent advances in the structural features, subcellular localization, biological functions, and molecular mechanisms of hCaf1 isoenzymes, with a focus on their roles in tumor progression. This work aims to facilitate a comprehensive understanding of hCaf1 family deadenylases.

LMR is a novel prognostic factor in r/r ATL and may provide useful information when considering mogamulizumab-based treatment.