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e addition of rIL-15 and, subsequently, confirmed in EBVaGC patient samples exhibiting increased expression of T cell surface markers and activation of immune co-stimulating pathways. Our findings suggest a mechanistic explanation for the clinical association of EBVaGC with a lower IL-15Rα expression, a better prognosis and an increased lymphocyte infiltration. We propose that in highly infiltrated GCs the IL-15/IL-15Rα complex on the GC cell surface may present IL-15 in trans to IL-2Rβ/γ-expressing immune cells to activate these cells