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. Author manuscript; available in PMC: 2011 Oct 1.
Published in final edited form as: Head Neck. 2010 Oct;32(10):1412–1421. doi: 10.1002/hed.21365

Figure 2.

Figure 2

A proposed model of cellular cascades triggered by activation of NK cells with cetuximab-coated HNSCC targets. Cetuximab-mediated NK cell-dependent tumor cell lysis results in the generation of EGFR-cetuximab immune complexes which are taken up by DC, processed and presented to TA-specific T cells. CTL recognize and eliminate tumor cells. T regulatory cells may down-regulate NK activity, DC functions and/or CTL activity, leading to tumor immune escape. In addition, defects in the antigen processing machinery component expression contribute to tumor escape from CTL recognition.