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. 2009 Sep 14;119(10):2976–2989. doi: 10.1172/JCI39518

Figure 8. Model for the involvement of SAP/NTB-A signaling in augmenting TCR signal strength for apoptosis.

Figure 8

Left: In previously activated T lymphocytes, TCR restimulation triggers increased association of NTB-A with SAP and colocalization with TCR-CD3 complexes, dislodging SHP-1 in the process. Exclusion of this phosphatase and potential recruitment of additional kinases ensures that optimal TCR signal transduction proceeds for the induction of downstream target genes such as FASL and BIM, which contribute to apoptosis execution. Right: In this fashion, SAP potentiates TCR signal strength past the required threshold for apoptosis induction in normal T cells. In SAP-deficient T cells, overall TCR signal strength is downmodulated below this threshold, allowing cells to escape deletion.