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Pancreatic cancer-associated stellate cells secrete soluble factors, such as interleukin-6 (IL-6), that promote the accumulation of myeloid-derived suppressor cells via a signal transducer and activator of transcription 3 (STAT3)-dependent mechanism. Targeting components of the IL-6/JAK/STAT3 signaling axis within the tumor stroma could therefore inhibit local immunosuppression and improve the efficacy of immunotherapeutic regimens against pancreatic cancer.
Mace et al. (Mon,) studied this question.