Analytical Validation of an Immunohistochemical 7-Biomarker Prognostic Assay (immunoprint) for Early-Stage Cutaneous Melanoma in Archival Tissue of Patients with AJCC v8 T2-T3 Disease.

Selected patients with early-stage melanoma have a "hidden high risk" of poor oncologic outcomes. They might benefit from clinical trials, and ultimately, if warranted by trial results, judicious everyday use of adjuvant therapy. A promising tool to identify these individuals is the immunoprint assay.

Inhibition of Mitochondrial Translation Ameliorates Imiquimod-Induced Psoriasis-Like Skin Inflammation by Targeting Vγ4+ γδ T Cells.

Psoriasis is an inflammatory skin disorder that is characterized by keratinocyte hyperproliferation in response to immune cell infiltration and cytokine secretion in the dermis. γδ T cells expressing the Vγ4 TCR chain are among the highest contributors of IL-17A, which is a major cytokine that drives a psoriasis flare, making Vγ4 γδ T cells a suitable target to restrict psoriasis progression. In this study, we demonstrate that mitochondrial translation inhibition within Vγ4 γδ T cells effectively reduced erythema, scaling, and skin thickening in a murine model of psoriatic disease.

Targeting ACC1 in T cells ameliorates psoriatic skin inflammation.

Psoriasis is a chronic inflammatory skin disease driven by the IL-23/IL-17 axis. It results from excessive activation of effector T cells, including T helper (Th) and cytotoxic T (Tc) cells, and is associated with dysfunctional regulatory T cells (Tregs). Acetyl-CoA carboxylase 1 (ACC1), a rate-limiting enzyme of fatty acid synthesis (FAS), directs cell fate decisions between Th17 and Tregs and thus could be a promising therapeutic target for psoriasis treatment.