In Vitro ADCC and NK Observations Sample Clauses

In Vitro ADCC and NK Observations. To characterize the potential for VTX-2337 to modulate immune function beyond the characterization in PD studies, immunophenotyping of peripheral blood and NK cell cytotoxic activity was assessed. These in vivo studies demonstrated that administration of VTX-2337 results in transient changes in blood cell populations consistent with cellular activation of neutrophils, NK cells, and T cells and may result in the transient extravasation of these latter cell populations from the blood compartment.[16] In addition, VTX-2337 stimulates the production of cytokines from mDC, monocytes, and NK cells in vitro.[17] VTX-2337 stimulates ADCC when used in combination with a variety of monoclonal antibodies of the IgG1 subclass including rituximab and traztuzumab.[17] More recently, in collaboration with Xx. Xxxxxx Xxxxxx at the University of Pittsburgh, it was demonstrated that VTX-2337 increases the cetuximab-mediated killing of SCCHN targets in an NK-dependent manner.[18] The TLR8 and NK-dependent enhancement of ADCC occurs in samples from patients of all three FcRγ3a genotypes, including those with the allele encoding the homozygous F/F variant that is associated with lower affinity for the Fc receptor. In addition, the stimulation of mDC and monocytes concurrent with cetuximab administration was tested to determine the promotion of development of EGFR-specific T cells via a mechanism referred to as ‘cross-priming’. Using a mixed culture model in vitro, tetramer analysis (using a molecular reagent that detects human leucocyte antigen-specific, EGFR peptide specific CD8+ T cells) demonstrated that VTX-2337 stimulates cross-priming and increases the number of EGFR-specific CD8+ T cells following cetuximab treatment. Taken together, the ability of VTX-2337 to stimulate the production of inflammatory cytokines (including XX-0, XX-00, XXXx, XX-00, and IFNg), the activation and stimulation of NK cells and ADCC, and the activation of the antigen processing and presentation of mDC and monocytes provide a strong rationale that this TLR8 agonist may enhance the activity of cetuximab in clinical studies.
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