Back

Crosslinked CXCR4 Signals Decreased Motility and Increased Adhesion of T Cells

Pearson, J.; Yang, J.-I.; Krivitsky, S.; Kelley, Z.; Fearon, D. T.

2025-06-05 immunology
10.1101/2025.06.04.652236 bioRxiv
Show abstract

Pancreatic ductal adenocarcinoma (PDA) is a highly aggressive cancer known for its ability to evade immune surveillance, primarily through mechanisms that prevent T cell infiltration. While the coating of cancer cells with the chemokine, CXCL12, is required for the exclusion of T cells, the precise molecular mechanisms behind the failure of T cell migration into the tumor remain unclear. In this study, we identify a potential mechanism by demonstrating that crosslinking CXCR4 is associated with decreased motility of T cells secondary to their adhesion to fibronectin. Using human lymphoblastoid T cells and primary human T cells, we show that polymeric CXCL12-induced crosslinked CXCR4 triggers the non-G i-dependent pathway of tyrosine phosphorylation of FAK-related proline-rich tyrosine kinase 2 (PTK2B) in T cells. This response is necessary for the decreased motility and increased adhesion of T cells. We also find that the downstream cellular reactions of this pathway is secondary to CXCR4-crosslinking and require the integrin subunit, 4, and TNF stimulation of TNFRSF1B. These findings provide insights into the mechanisms mediating the exclusion of T cells from nests of PDA cells and further support therapeutic strategies aimed at blocking the interaction of CXCR4 on T cells with the CXCL12-coating of PDA cells.

Matching journals

The top 8 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.