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Enhanced apoptosis of T cells in common variable immunodeficiency (CVID): role of defective CD28 co-stimulation.

Abstract：

:CVID is a primary immune disorder in which hypogammaglobulinaemia may be associated with a number of T cell defects including lymphopenia, anergy, impaired lymphocyte proliferation and deficient cytokine secretion. In this study we show that T cells of CVID subjects, in comparison with control T cells, undergo spontaneous apoptosis in culture and markedly accelerated apoptosis after gamma-irradiation. Although costimulation of the CD28 receptor following engagement of the TCR/CD3 receptor normally provides a second signal necessary for IL-2 secretion, CD28 costimulation in CVID does not significantly increase IL-2 production, nor does this combination of activators enhance the survival of irradiated CVID T cells, as it does for cultured normal T cells. Addition of IL-2 enhances CVID T cell survival, suggesting that the IL-2 signalling pathways are normal. CVID T cells have similar expression of Bcl-2 to control T cells. CD3 stimulation up-regulates T cell expression of bcl-xL mRNA for normal T cells, but anti-CD28 does not augment bcl-xL expression for CVID subjects with accelerated apoptosis. Defects of the CD28 receptor pathway, leading to cytokine deprivation and dysregulation of bcl-xL, could lead to poor T cell viability and some of the cellular defects observed in CVID.

journal_name

Clin Exp Immunol

journal_title

Clinical and experimental immunology

authors

Di Renzo M,Zhou Z,George I,Becker K,Cunningham-Rundles C

doi

10.1046/j.1365-2249.2000.01239.x

subject

Has Abstract

pub_date

2000-06-01 00:00:00

pages

503-11

issue

3

eissn

0009-9104

issn

1365-2249

pii

cei1239

journal_volume

120

pub_type

杂志文章

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