Fig. 1.
Cellular proliferation in MLR is effectively attenuated by mPEG-modification of either the responder (main graph) or stimulator (insert) PBMC population. As shown, pegylation of responder cells leads to a mPEG dose-dependent loss of cellular proliferation in response to a disparate MHC class II stimulator PBMC population. Insert: Increasing responder cell numbers does not overcome the antiproliferative effects of mPEG-modification. Shown is increasing numbers of unmodified responder cells exposed to 2.5 × 105 pegylated (2.4 mmol/L per 4 × 106 PBMC) stimulator PBMC. Cell proliferation was determined by 3H-thymidine incorporation into the DNA of the responder cells after 4 days exposure to stimulator cells (irradiated to prevent cell replication). Longer incubations (7 days) were also performed on human PBMC MLR yielding similar results, but higher control counts per minute (CPM). The results shown are the mean ± standard deviation (SD) of triplicate samples from a representative experiment from over 20 individual studies. The main graph uses donors 2 and 3 (responder), while the insert uses donors 2 and 4 (responder). All values for the mPEG-derivatized cells different from control PBMC at P < .0001.