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However, the living cell binding evaluation showed that rituximab could scarcely bind to these cells.
Since the membrane of apoptotic, hypoxic and ischemic cells depolarised, annexin V and lactadherin most likely bind to these cells with a higher affinity than to cells with preserved membrane potential.
Binding analysis using flow cytometry of the porcine CTLA-4 fusion toxins to LCL13271 cells also demonstrated that the non-N-glycosylated porcine CTLA-4 isoforms bind to these cells with higher affinity compared to the glycosylated fusion toxin.
Through competition, they prevent pathogenic auto-antibodies to bind to these cells and prevent immune activation [ 18].
To determine whether preadipocytes and adipocytes inhibit ADCC by sequestering the antibody, we first determined the ability of trastuzumab to bind to these cells.
SfbI was found to bind to these cells, via the fibrinogen on their surfaces: again this depended on the thioester bond in SfbI.
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In contrast, CCRCM1 did not bind to these cell walls although it did bind to non-thickened cell walls of the vascular tissue (not shown).
Among the lectins that were observed to bind to these cell lines, four (namely, RCA-I, Triticum vulgaris agglutinin (WGA), Wisteria floribunda agglutinin (WFA) and Sambucus nigra agglutinin I (SNA-I)) were found to show noticeably different extents of binding to different cell lines.
Antibodies from the patients bound to these cells in 17 of 20 samples.
The Eu-labeled ligand bound to these cells with an affinity similar to that of unlabeled NDP-α-MSH and was used to optimize a competitive binding assay.
Furthermore, flowcytometric analysis confirmed that these clones expressed human CD2 and that CD58-BV bound to these cells (Fig. 5B).
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