685 Reprogramming of tumor-associated macrophages with anti-PD-L1 & lenalidomide in cutaneous T cell lymphoma

Abstract

M2-like tumor-associated macrophages (TAMs) promote the growth of cutaneous T cell lymphoma (CTCL) by inducing immunosuppression. Little is known about the underlying mechanisms of PD1+ M2-like TAM phenotypes in CTCL. Understanding the mechanisms of macrophage reprogramming will identify novel therapeutic targets to induce anti-tumor responses. We used multiplex immunofluorescence on CTCL skin samples demonstrating co-localization of PD1 on CD163+ M2 macrophages. RNA-seq analysis on tissue sections from same CTCL specimens revealed an up-regulation of the TLR/NF-κB and JAK/STAT signaling pathways.