Table 1.

Dual role of key components of pancreatic tumor microenvironment

Component	Pro-tumor effects	Anti-tumor/limiting effects
T lymphocytes	CD4+ T cell supported cancer progression by secreting IL-17 and IL-27 [551, 552]	Cytotoxic TILs induced tumor regression [553, 554]
Regulatory T lymphocytes (Tregs)	Treg suppressed immunity against early stage pancreatic intraepithelial neoplasms [555]	Treg depletion led to accelerated tumor progression [104]
B lymphocytes	B cells supported tumor progression/proliferation by secreting IL-35 and activating immunosuppressive TAMs [556, 557]	Insufficient data
Myeloid cells	CD11b+ myeloid cells are required for oncogenic Kras-driven PanIN formation [165, 166, 558]	Reinvigorating dysregulated myeloid cells in therapeutic settings (e.g., using CD40 agonist) [130, 407, 431, 559]
CAF	Regulating tumor metabolism for cancer cell proliferation and suppressing anti-tumor immunity [35, 560–563]	Increased matrix deposition and forming a dense and stiff matrix around early PDAC cells [242, 564, 565]
ECM	Supporting cancer cell proliferation and migration [566, 567]	Cancer-cell-derived fibrillar collagen and type I collagen restrains tumor growth [568, 569]

CAF: Cancer-associated fibroblast, ECM: Extracellular matrix, PanIN: Pancreatic intraepithelial neoplasia, PDAC: Pancreatic ductal adenocarcinoma, TAMs: Tumor-associated macrophages, TILs: Tumor-infiltrating lymphocytes