Soluble Fcγ receptor IIIb alters the function of polymorphonuclear neutrophils but extends their survival
✍ Scribed by Véronique Durand; Jacques-Olivier Pers; Yves Renaudineau; Pierre Youinou; Christophe Jamin
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 184 KB
- Volume
- 31
- Category
- Article
- ISSN
- 0014-2980
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✦ Synopsis
We have established that polymorphonuclear neutrophil (PMN)-binding anti-Fc + receptor IIIb (Fc + RIIIb) autoantibodies (autoAb) inhibit the function of these cells but extend their survival. Here, we show that recombinant Fc + RIIIb (rFc + RIIIb), as well as purified Fc + RIIIb (pFc + RIIIb), deteriorated the PMN adherence and respiratory burst in a dose-dependent manner. Furthermore, rFc + RIIIb and pFc + RIIIb reduced the level of annexin V-binding PMN from 23.6 ± 1.6 % to 6.3 ± 1.0 and 11.0 ± 1.0 %, respectively, while human serum albumin exerted no effects. Incubation of rFc + RIIIb with those autoAb binding to soluble Fc + RIIIb resulted in the attachment of such immune complexes (IC) to the cells, thereby also delaying apoptosis (44.9 ± 5.9 versus 18.0 ± 2.0 % annexin V-binding PMN after 16 hours). Soluble Fc + RIIIb, in concert with Fc + RIIIb/anti-Fc + RIIIb IC, produced similar effects in that the percentage of annexin V-binding PMN declined to 16.0 ±1.9 %. It was thus suggested that Fc + RIIIb/anti-Fc + RIIIb IC inserted the Fc region of their IgG into the membrane Fc + RIIIb. Such an interpretation is consistent with our finding that, whereas aggregated IgG and anti-Fc + RIIIb monoclonal Ab prevented membrane Fc + RIIIb/IC interaction, neither soluble Fc + RIIIb, nor anti-Fc + RII did so. We conclude that the function and the life span of PMN are influenced synergistically by soluble Fc + RIIIb and anti-Fc + RIIIb autoAb.