LALA is a b12 variant deficient in Anti-Mouse CD209b Antibody Formula binding to Fc receptors. Overall, the effector Anti-Mouse CD11b Antibody manufacturer function assays Anti-Mouse CD28 Antibody References clearly demonstratethat the in vitro antiviral Fc RIIIa-dependent activity of NFb12 is superior to that of wild-type b12. (A) HIV SF162 gp120 ELISA. Wild-type b12 and NFb12 bound HIV gp120 with similarapparent affinities. Values are mean and standard deviations (n 2). (B) Cell surface binding of wild-type b12 and NFb12 to HIV JRFL envelope. Wild-type b12 and NFb12 bound cell surface-expressed HIV JRFL envelope with comparable potencies. Binding curves were generated by plotting the mean fluorescence intensity (MFI) of antigen binding as a function of PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/25782580?dopt=Abstract antibody concentration. Values are mean and standard deviations (n 2). (C) Single-round SHIVSF162P3 pseudovirus neutralization assay. Wild-type b12 and NFb12 neutralized SHIVSF162P3 pseudovirus with comparable potencies (IC50 for b12, 0.24 g/ml; IC50 for NFb12, 0.38 g/ml). Control IgG1 antibody DEN3 did not neutralize virus. Values are mean and standard deviations (n 6).jvi.asm.orgJournal of VirologyNFb12 Does Not Improve Protection against SHIVFIG 4 NFb12 and b12 half-lives in rhesus macaque. (A) Three animals were administered 5 mg/kg NFb12 i.v., and serum levels were d.
S were infected with SHIVSF162P3 for 48 h before incubation with effector cells and antibodies. Viral inhibition was measured after 7 days by a p27-specific ELISA. (A) NFb12 showed a 10-fold enhanced potency in viral inhibition compared to wild-type b12 in the presence of PBMCs (IC50 for b12, 4.37 g/ml; IC50 for NFb12, 0.43 g/ml). Values are mean and standard deviations (n 2). (B) Wild-type b12 and NFb12 showed comparable potencies in viral inhibition in the presence of monocytes (IC50 for b12, 3.97 g/ml; IC50 for NFb12, 6.97 g/ml). Values are mean and standard deviations (n 2). (C) ADCC assay. Killing of target cells is seen as a decrease in luciferase activity (RLU).S were infected with SHIVSF162P3 for 48 h before incubation with
S were infected with SHIVSF162P3 for 48 h before incubation with effector cells and antibodies. Viral inhibition was measured after 7 days by a p27-specific ELISA. (A) NFb12 showed a 10-fold enhanced potency in viral inhibition compared to wild-type b12 in the presence of PBMCs (IC50 for b12, 4.37 g/ml; IC50 for NFb12, 0.43 g/ml). Values are mean and standard deviations (n 2). (B) Wild-type b12 and NFb12 showed comparable potencies in viral inhibition in the presence of monocytes (IC50 for b12, 3.97 g/ml; IC50 for NFb12, 6.97 g/ml). Values are mean and standard deviations (n 2). (C) ADCC assay. Killing of target cells is seen as a decrease in luciferase activity (RLU). NFb12 showed 10-fold enhanced killing of target cells compared to wild-type b12 (IC50 for b12, 1.3 g/ml; IC50 for NFb12, 0.13 g/ml). LALA and DEN3 did not mediate killing of infected cells as LALA did not recruit effector cells and DEN3 did not recognize HIV gp120. Values are the average of two independent experiments done in triplicate.