• Media type: E-Article
  • Title: T cells from patients with Hodgkin's disease have a defective T-cell receptor zeta chain expression that is reversible by T-cell stimulation with CD3 and CD28
  • Contributor: Renner, C; Ohnesorge, S; Held, G; Bauer, S; Jung, W; Pfitzenmeier, JP; Pfreundschuh, M
  • Published: American Society of Hematology, 1996
  • Published in: Blood, 88 (1996) 1, Seite 236-241
  • Language: English
  • DOI: 10.1182/blood.v88.1.236.bloodjournal881236
  • ISSN: 0006-4971; 1528-0020
  • Keywords: Cell Biology ; Hematology ; Immunology ; Biochemistry
  • Origination:
  • Footnote:
  • Description: <jats:p>To investigate the mechanisms underlying the deficiency of T lymphocytes from patients with Hodgkin's disease, we investigated the expression of the T-cell receptor (TCR) zeta chain in patients with Hodgkin's disease. By flow cytometry using an anti-zeta chain monoclonal antibody, peripheral blood T lymphocytes from patients with untreated Hodgkin's disease were shown to express decreased levels of the TCR zeta chain. After stimulation by combined CD3 and CD28 cross- linking, T cells from Hodgkin's disease patients upregulated zeta chain protein expression to normal values within 48 hours and achieved a cytolytic potential and levels of interleukin (IL)-2 secretion that were not different from T cells obtained from healthy controls. These results show that downregulation of the TCR zeta chain in Hodgkin's T lymphocytes is a reversible event. Costimulation of CD3 and CD28 is a novel approach for overcoming the T-cell deficiency in Hodgkin's disease and might be exploited clinically. As upregulation of the zeta chain can also be achieved using bispecific monoclonal antibodies (BI- MoAbs) with specificity for tumor antigens and CD3 and CD28, respectively, an immunotherapy with CD3/CD30 and CD28/CD30 Bi-MoAbs may overcome and should therefore, not be jeopardized by the inherent T- cell deficiency in patients with Hodgkin's disease.</jats:p>
  • Access State: Open Access