Source: Annual Congress 2002 - Cellular reactions in allergy in humans and animals
Disease area: Airway diseases

Abstract

Fas-receptor levels and mechanisms of Fas-mediated PBL apoptosis were determined in ABA patients and donors. Fas-receptor and FasL expression and apoptosis markers in various resting and activated PBL populations were determined using dual- and three-color fluorescence by flow cytometry method. Apoptosis was measured by decrease of transmembrane mitochondrial potential, out plasma membrane phosphatidylserine exposure, BcL-2 expression and DNA fragmentation.
It was shown the significant decrease of Fas-receptor expression on CD4+- and CD8+-PBL in ABA patients. Expression of FasL and activation markers (CD25, HLA-DR) in PBL were low and in most cases not detected (no difference between donors and ABA). Incubation of resting PBL with anti-Fas mAbs didn[scquote]t induce apoptosis (although the high levels of Fas). TCR-activation of PBL (anti-CD3-mAbs) significantly increased levels of Fas+-, CD25+- and HLA-DR+-cells (not FasL+-cells) in donors and ABA patients and induced their responsibility to Fas-mediated apoptosis which however was significantly lower in ABA patients. This resistance was not dependent of glucocorticoid (GC)-treatment of ABA.
We conclude that PBL sensitivity to Fas-mediated apoptosis highly depends only of functional (activation) state of PBL (but not of Fas expression levels). Furthermore antigen(Ag)-activated PBL from ABA patients show their resistance to Fas-mediated apoptosis which is not GC-dependent and may lead to the chronic inflammation through the defect of T-cell elimination after the response to Ag.

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Citations should be made in the following way:
S. V. Boichuk, I. G. Mustafin, R. S. Fassahov (Kazan, Russia). T cell resistance to Fas-mediated apoptosis during atopic bronchial asthma (ABA). Eur Respir J 2002; 20: Suppl. 38, 307

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