In mouse models, TACI signaling increases the movement of chronic lymphocytic leukemia cells to the spleen and promotes an immune-suppressing environment that allows the tumor to survive.
Mechanism
Synthesis from 1 study
TACI activation tells leukemia cells to travel to the spleen and release signals that turn off immune cells. Once there, the cancer cells live undisturbed because the immune system cannot attack them.
Most probable mechanism
When TACI is activated, leukemia cells move to the spleen and release signals that shut down immune cells, allowing the cancer to survive unchecked.
TACI receptor binding by BAFF or APRIL ligands activates the NF-κB signaling pathway in chronic lymphocytic leukemia cells
NF-κB activation increases expression of immunosuppressive molecules including IL-10, PD-L1, and PD-L2 on leukemia cells
Elevated IL-10, PD-L1, and PD-L2 suppress T-cell activation and function in the spleen
Leukemia cells migrate to and accumulate in the spleen due to TACI-dependent chemotactic signals
Splenic accumulation of leukemia cells and sustained immunosuppression creates a microenvironment that protects tumor cells from immune destruction
Evidence from Studies
Supporting (1)
Community contributions welcome
Abstract PR-06: Disrupting TACI signaling to restore immune balance: harnessing translational opportunities at the intersection of cancer and autoimmunity
Contradicting (0)
Community contributions welcome
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