MHCII+ cancer-associated fibroblasts promote antitumor immunity in pancreatic cancer

IFN{gamma}-driven MHCII expression on cancer-associated fibroblasts is linked to antitumor control in orthotopic pancreatic cancer models, especially when Tregs are depleted.

• Why it matters: MHCII+CAFs are often viewed as immunosuppressive, but their role in pancreatic ductal adenocarcinoma may depend on immune context and fibroblast–T cell interactions.
• What they did: In orthotopic PDAC models, conventional CD4+ T cells and IFN{gamma} increased MHCII+CAFs; acute Treg depletion in Foxp3DTR mice showed Tregs limit MHCII+CAF abundance, and fibroblast MHCII was required for CD4-driven control.
• The result: Treg ablation enables CD4 T cell responses that suppress PDAC progression and metastasis, implying MHCII+CAF biology can be harnessed to promote adaptive antitumor immunity in PDAC.

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