Establishment of a leukemic T-cell line expressing a conformationally different but functional IL-2R (Meeting abstract). NLM AIDSLINE Important note: Information in this article was accurate in 1993. The state of the art may have changed since the publication date.

Click here to return to AIDSLINE main menu
DonateNow
Print this Article


Establishment of a leukemic T-cell line expressing a conformationally different but functional IL-2R (Meeting abstract).

Proc Annu Meet Am Assoc Cancer Res; 34:A322 1993. Unique Identifier : AIDSLINE ICDB/93691308
Sahraoui Y; Thedoropoulo M; Ammar A; Clemenceau C; Jasmin C; Georgoulias V; INSERM U268, Hopital Paul Brousse, Villejuif, France


Abstract: Leukemic cells from a 45-yr-old male patient with an acute lymphoblastic leukemia of T-cell origin were cultured in vitro in the absence of any added growth factor for up to 2 yr and a continuous cell line (NOI-90) was established. Phenotypic and karyotypic analysis of NOI-90 cells revealed only small differences from initial leukemic cells. NOI-90 cells expressed a low amount of the IL2R alpha and IL-2R beta of IL-2R, respectively, and scatchard analysis revealed the presence of a small number of high-affinity IL-2R, which was unchanged during a 18-mo period. The NOI-90 cells secrete a biological IL2 activity and the specific mRNA could be detected by PCR. Although added IL2 could not induce cell proliferation, monoclonal antibodies (MoAb) against IL2R alpha, IL2R beta and IL2, as well as an immunosuppressive molecule, p29, secreted by HIV-infected adherent cells, could inhibit spontaneous cell proliferation in a dose-dependent manner. The effect of MoAb against IL-2R beta on the spontaneous cell proliferation is not observed on normal activated T-cells (PHA-blasts) in the same conditions. The antiproliferative effect at 37 C of anti-IL2R beta is quite striking, since in normal PHA-blasts, 3.58 pM IL2 displaces the moAbs, whereas in NOI-90 cells 3580 pM, IL2 does not displace the anti-IL2R beta. These data suggest in a particular subset of T-ALL patients, the existence of an heterodimer with a different configuration defining a thousand increased affinity of this epitope for this MoAb.
Keywords: Cell Division/GENETICS Cell Line Gene Expression Regulation, Leukemic/*PHYSIOLOGY Human Leukemia, T-Cell, Acute/*GENETICS/PATHOLOGY Male Middle Age Protein Conformation Receptors, Interleukin-2/*GENETICS ABSTRACTKWDcelldivision/geneticscelllinegeneexpressionregulation,leukemic/KWDphysiologyhumanleukemia,t-cell,acute/KWDgenetics/pathologymalemiddleageproteinconformationreceptors,interleukin-2/KWDgeneticsabstract
930830
M9380837

Copyright © 1993 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

AEGiS is a 501(c)3, not-for-profit, tax-exempt, educational corporation. AEGiS is made possible through unrestricted funding from Boehringer Ingelheim, Bridgestone/Firestone Charitable Trust, Bristol-Myers Squibb Company, Elton John AIDS Foundation, Gill Foundation, the National Library of Medicine, Quest Diagnostics, Roche and Trimeris, and donations from users like you. Always watch for outdated information. This article first appeared in 1993. This material is designed to support, not replace, the relationship that exists between you and your doctor.

AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.

Copyright ©1980, 1993. AEGiS. All materials appearing on AEGiS are protected by copyright as a collective work or compilation under U.S. copyright and other laws and are the property of AEGiS, or the party credited as the provider of the content. .