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CXCL10

Cytosolic-DNA-Mediated STING-Dependent Inflammation Contributes to the Progression of Psoriasis

[Journal of Investigative Dermatology] Stimulator of IFN genes (STING) is a universal receptor that recognizes cytosolic DNA and triggers innate immune activation. Investigators elucidated the role of STING in the inflammation during psoriasis.

CXCL9 as a Key Biomarker of Vitiligo Activity and Prediction of the Success of Cultured Melanocyte Transplantation

[Scientific Reports] Scientists investigated the potential biomarkers of vitiligo by evaluating the disease activity and curative effect of autologous cultured pure melanocyte transplantation on patients.

Role of CXCL10 in the Progression of In Situ to Invasive Carcinoma of the Breast

[Scientific Reports] Scientists performed immune profiling to compare immune-related gene expression between ductal carcinoma in situ and invasive carcinoma of the breast using nCounter PanCancer immune Profiling Panel and found that CXCL10 was the most significant gene that had the highest difference in expression between them.

Pro-Inflammatory β Cell Small Extracellular Vesicles Induce β Cell Failure through Activation of the CXCL10/CXCR3 Axis in Diabetes

[Cell Reports] Scientists reported that pro-inflammatory β cell small extracellular vesicles induced β cell dysfunction, promoted a pro-inflammatory islet transcriptome, and enhanced recruitment of CD8+ T cells and macrophages.

Lenvatinib Enhances T Cell Immunity and the Efficacy of Adoptive Chimeric Antigen Receptor-Modified T Cells by Decreasing Myeloid-Derived Suppressor Cells in Cancer

[Pharmacological Research] The antitumour activity of lenvatinib in immunocompetent and immunodeficient mice was compared to determine the role of T cell immunity. The antitumour activity of T cells was analysed by cytokine production and adoptive T cell therapy.

Malaria Parasites Both Repress Host CXCL10 and Use It as a Cue for Growth Acceleration

[Nature Communications] Researchers showed a Pf ‘decision-sensing-system’ controlled by CXCL10 concentration. High CXCL10 expression prompted P. falciparum to initiate a survival strategy via growth acceleration.

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