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• W1972789617 abstract "714 We have previously described the inhibition of allospecific responses in the MLR by IVIG. We suggested that IVIG interferes with a early activation signal(s) of the MLR primarily through stimulator cells. We also suggested that the inhibitory effect is mediated primarily by the F(ab')2 portion of IgG since Gamma-Venin (GV) consisting of F(ab')2 of IgG inhibited the MLR as effectively as IVIG. To confirm the inhibitory effect of GV on an early activation signal(s) in the MLR, we performed two experiments. In the 1st experiment, the MLR was initiated with IVIG or GV, the additives were washed out at various time points and then cells recultured for the remainder of the MLR. In the 2nd experiment, IVIG or GV were added at various time points post MLR. In addition, we compared the effect of IVIG vs. GV on PHA-stimulated cell proliferation in PBMCs. Finally, we examined the effect of IVIG and GV on gene expression of cytokines (TNFα, IL-2, IFNγ and TGF β1) and cell surface molecules (IL-2R, B7-1, B7-2, ICAM-1, LFA-1, CTLA-4, CD28, CD40, CD40L, MHC Class I and Class II) required for the MLR using RT-PCR and flow cytometry. Result: Nearly maximal inhibition of cell proliferation was seen even when IVIG was washed out as early as 5 hrs post MLR. In marked contrast, the suppressive effect of GV on the MLR was significantly reduced when it was washed out as late as 72 hrs. The later IVIG was added to the MLR culture, the less suppression was seen. No significant inhibition was detected when IVIG was added at 48 hours. In contrast, GV showed nearly maximal inhibition even when it was added at 72 hrs. GV showed significant suppressive effects on PHA-stimulated cell proliferation while IVIG did not (70% vs. 0% at 10 mg/ml, p<0.05). IVIG reduced expression of MHC class II by 30-50% in the MLR analyzed by flow cytometry while GV has minimum or no effect. IVIG and GV have minimum or no effect on MHC class I, CD40 and CD40L expression. TNFα mRNA expression was increased by IVIG, but not by GV. mRNA expression of IL-2, IFNγ and TGFβ1 were not significantly affected by IVIG and GV. mRNA expression of IL-2R was suppressed by IVIG and with GV to a lesser degree. Both IVIG and GV have minimum or no effect on mRNA expression of other surface molecules examined. Conclusions: The mechanisms responsible for the inhibitory effects of whole IgG and the F(ab')2 portion of IgG on cell proliferation in the MLR are different: 1) The F(ab')2 of IgG interferes with events occurring in a later stage of the MLR. In contrast, the whole IgG molecules interfers with an early activation signal in the MLR presumably through Fc mediated events, 2) Reduction of MHC class II expression on antigen presenting cells may be an important mechanisms responsible for the inhibitory effect of IVIG in the MLR." @default.
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• W1972789617 date "1998-05-01" @default.
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• W1972789617 title "POOLED HUMAN GAMMAGLOBULIN (IVIG) AND F(ab')2 FRAGMENTS OF IVIG INHIBIT THE MIXED LYMPHOCYTE REACTION (MLR) THROUGH DIFFERENT MECHANISMS" @default.
• W1972789617 doi "https://doi.org/10.1097/00007890-199805131-00710" @default.
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