The results revealed that Trp176, Phe178, and Arg181 are essential amino acids for the recognition by S15040E. These results showed the involvement of the ECL2 of mCCR1 in the recognition by S15040E.
Commensal dysbiosis could promote CRLM development via CCL6/CCR1 signaling. Targeting this signaling axis could be an effective method to inhibit CRLM by regulating the TME.
scRNA-seq identified the intricate tumor immune microenvironment, highlighting the pivotal roles of TAMs and mast cells in gastric cancer peritoneal metastasis. The CCL5-CCR1 pathway emerged as a potential immune checkpoint, offering novel insights for future immunotherapeutic and targeted therapeutic strategies in the treatment of gastric cancer peritoneal metastasis.
5 months ago
Journal • IO biomarker
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STAT3 (Signal Transducer And Activator Of Transcription 3) • S100A9 (S100 Calcium Binding Protein A9) • C1QB (Complement C1q B Chain) • CCR1 (C-C Motif Chemokine Receptor 1) • CD1C (CD1c Molecule)
Our data highlight several CRs as candidate prognostic markers and potential therapeutic targets in the context of POD24, warranting further investigation in larger, prospective cohorts. Trial Registration: The authors have confirmed clinical trial registration is not needed for this submission.
In addition, we conducted a drug screening targeting CCR1 and identified Jervine as a potential CCR1 degrader. In summary, this study uncovers the relationship between CCL15-CCR1 axis and ESCC progression and provides insights into potential therapeutic strategies targeting this pathway.
Our study revealed complex changes in the tumor microenvironment of patients with CRLM and T2D. In particular, a novel mechanism was identified by which hyperglycemia regulates immunosuppression: the CCL3-CCR1 signaling axis. This finding offers a novel potential therapeutic target for patients with CRLM and T2D and provides an important theoretical basis for the future prediction of the prognosis of these patients.
The chemokine signaling pathway plays a role in the malignant transformation of LGBLEL. The decreased expression of CCL28 and CXCL17, coupled with the increased expression of CCR1, may be linked to the progression of LGBLEL into lymphoma.
Our work identifies CCR1 as a potential immune check point regulator of PD-L1 and may cause T cell exhaustion and cytotoxicity suppression in ESCC micro-environment and highlights the potential value of CCR1 as therapeutic target of immunotherapy. Implications: The esophageal microbial environment and its metabolites significantly affect the outcome of immunotherapy for ESCC.
MIP-1α and CCR1 were upregulated in human small bowel injury samples as compared with the normal ileal mucosa tissues. In conclusion, our findings demonstrated that OMT could alleviate NSAID-associated small bowel mucosal injury by inhibiting MIP-1γ/CCR1 signalling and regulating gut microbiota.
Our data indicate that macrophages are implicated in the development and progression of testicular inflammation by expressing CCR2 and activin A, which ultimately remodel the chemokine/chemokine receptor network and recruit other immune cells to the site of inflammation. Consequently, inhibition of CCR2 or activin A could serve as a potential therapeutic strategy for reducing testicular inflammation.