Figure 2.

Therapeutic opportunity for anti-MICA/B Ab. Administration of anti-MICA/B Ab may trigger CD16-dependent ADCC by NK cells when these Ab recognize cell surface-expressed MICA/B, contributing to tumor cell elimination. Ab that do not interfere with the binding of NKG2D to MICA/B also would trigger NKG2D-dependent NK cell-mediated cytotoxicity, further contributing to tumor cell elimination. Moreover, recognition of sMICA/B by these therapeutic anti-MICA/B Ab would lead to the formation of immune complexes that would be removed by macrophages upon recognition through CD16, CD32 and CD64. This scavenging of sMICA/B will consequently interfere with tumor immune escape (immunoevasion).