Journal: Cellular Oncology (Dordrecht, Netherlands)
Article Title: CXCL12 derived from cancer-associated fibroblasts mediates dysfunctional intratumoral adaptive immunity in diabetic pancreatic adenocarcinoma
doi: 10.1007/s13402-026-01165-x
Figure Lengend Snippet: Overexpressed CXCL12 exacerbated in vivo adaptive immune migration and dysfunction in diabetic PAAD. A-C Schematic diagram of animal experiment and harvested subcutaneous tumors from different groups ( n = 6). D-E Estimation of intratumoral CD19 + B cells and CD8 + T cells distribution by IHC ( n = 6). Scale bar: 50 µm. F CD22 + percentage of CD19 + B cells by flow cytometry ( n = 5). G TIGIT expression of intratumoral CD8 + T cells in mPSC oe-NC , mPSC oe-CXCL12 , and mPSC oe-CXCL12 +plerixafor groups ( n = 5). All data were expressed as mean ± SD
Article Snippet: Harvested tumor paraffin samples were incubated with primary antibodies against CD8, TIGIT, CD19, CD22, Desmin, and CXCL12 (Cell Signaling Technology, Danvers, USA).
Techniques: In Vivo, Migration, Flow Cytometry, Expressing