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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: Tumor immune microenvironment-based therapies in pancreatic ductal adenocarcinoma: time to update the concept

Fig. 4

Various CAFs in PDAC, CAF function, and plasticity. CAFs in the TIME of PDAC are mainly divided into iCAFs, myCAFs and apCAFs, which perform different functions. These three classical subtypes can be further subdivided by different markers. New subtypes, such as csCAFs and meCAFs, are also being discovered. Tumor cells can promote the activation of iCAF by upregulating the expression of IL-1, and TGF-β signaling can induce the proliferation of myCAF by antagonizing this process. This CAF plasticity suggests that we can achieve the purpose of treatment by reprogramming CAFs. CAF: cancer-associated fibroblast; iCAF: inflammatory CAF; myCAF: myofibroblastic CAF; apCAF: antigen-presenting CAF; LRRC15: leucine-rich repeat containing 15; csCAF: complement-secreting CAF; meCAF: CAF with a highly activated metabolic state

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