Cell surface expression of CR1 is down-regulated on purified human MO exposed to recombinant IFNγ. Quantitation of receptor numbers using 125I-Fab monoclonal antiCR1 showed that MO freshly isolated from one individual expressed 8571 CR1/cell. When cultured in suspension with monoclonal antiIFNγ under endotoxin free conditions, MO expressed 12,143 CR1/cell after 3 days and 11,500 CR1/cell after 6 days. However, when MO were exposed to 100 IRU/ml IFNγ receptor levels dropped to 4970 after 3 days in culture (41% of control) and to 3200 after 6 days (28% of control). These results were also confirmed by rosette analysis and flow cytometry. Whereas 78% of control cultured MO formed strong rosettes with erythrocytes bearing C3b, 17% of the IFNγ-treated population rosetted only weakly. FACS analysis using monoclonal antiCR1 showed that while control cells from a second donor displayed a mean channel fluorescence (MCF) of 43.9 and carried 21,600 CR1/cell, IFNγ-treated MO had a MCF of only 15.2. This down-regulation was selective for CR1 since IFNγ induced a 98 channel increase in HLA-DS expression and a 61 channel increase of Fc receptor levels in the same cells. Bacterial endotoxin, which mimics many of the MO-activating properties of IFNγ also down-regulated MO CR1. These results suggest that IFNγ may play a role in regulating CR1 expression on MO surfaces.
|Pages (from-to)||No. 8564|
|State||Published - Jan 1 1985|