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Titolo:
Enhanced apoptosis of T cells in common variable immunodeficiency (CVID): role of defective CD28 co-stimulation
Autore:
Di Renzo, M; Zhou, Z; George, I; Becker, K; Cunningham-Rundles, C;
Indirizzi:
Mt Sinai Med Ctr, Div Clin Immunol, New York, NY 10029 USA Mt Sinai Med Ctr New York NY USA 10029 in Immunol, New York, NY 10029 USA
Titolo Testata:
CLINICAL AND EXPERIMENTAL IMMUNOLOGY
fascicolo: 3, volume: 120, anno: 2000,
pagine: 503 - 511
SICI:
0009-9104(200006)120:3<503:EAOTCI>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
COSTIMULATORY SIGNAL; B-CELLS; CD28-DEFICIENT MICE; HUMAN-LYMPHOCYTES; INTERFERON-GAMMA; DNA-SYNTHESIS; ANTIGEN; INTERLEUKIN-2; EXPRESSION; RECEPTOR;
Keywords:
immunodeficiency diseases; T lymphocytes; apoptosis; CD28; Bcl-xl; co-stimulatory molecules;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Di Renzo, M Policlin Le Scotte, Ist Semeiot Med, I-53100 Siena, Italy Policlin Le Scotte Siena Italy I-53100 I-53100 Siena, Italy
Citazione:
M. Di Renzo et al., "Enhanced apoptosis of T cells in common variable immunodeficiency (CVID): role of defective CD28 co-stimulation", CLIN EXP IM, 120(3), 2000, pp. 503-511

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 dysregulationof bcl-xL, could lead to poor T cell viability and some of the cellular defects observed in CVID.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/11/20 alle ore 10:37:48