Immunological Reviews – Figure 4

Fig. 4. Regulation of CTLA-4 mediated growth arrest by the galectin-glycoprotein lattice.

Galectin binding to N-glycans attached to CTLA-4 enhances surface retention by opposing endocytic loss, resulting in sustained and increased arrest signaling. CTLA-4 has only two N-glycan sites and undergoes rapid degradation due to high constitutive endocytosis rates via AP-2-mediated targeting into clathrin-coated pits. TCR signaling increases metabolic flux to N-glycan branching, promoting incorporation of CTLA-4 into the galectin-glycoprotein lattice to sustain surface retention and augment growth arrest.

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