Fisher, R. I. ; Bates, S. E. ; Bostick-Bruton, F. ; Tuteja, N. ; Diehl, V. (1984) Neoplastic cells obtained from Hodgkin's disease function as accessory cells for mitogen-induced human T-cell proliferation responses The Journal of Immunology, 132 (5). pp. 2672-2677. ISSN 0022-1767
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Official URL: http://www.jimmunol.org/content/132/5/2672.short
Abstract
Purified human peripheral blood T cells that have been depleted of Ia- bearing cells and adherent cells do not proliferate in response to concanavalin A. The addition of as few as 1% radiated L428 tumor cells restores the proliferative capacity of the T cells. The L428 cell line is a long-term tissue culture line of Reed-Sternberg cells obtained from a patient with Hodgkin's disease. The proliferation of the T cells plus the L428 cells follows the same kinetics and has the same response to varying doses of mitogen as either unfractionated mononuclear leukocytes or purified T cells plus allogeneic adherent cells. The L428 cells are 30 times more potent as accessory cells than allogeneic adherent cells. The accessory cell function of the L428 cells is not blocked in cultures containing anti-Ia antibody. Neither supernatant from the L428 cell cultures nor human IL 1 replaces the accessory cells. The ability of the L428 cells to restore the proliferative capacity of purified T cells isolated from patients with active Hodgkin's disease was also studied. Patients with early stages of the disease had normal proliferative responses in the presence of the L428 accessory cells. However, the proliferative response of the poor prognosis, advanced-stage patients was reduced as compared to age- and sex-matched controls, supporting a deficit in their T cell function. The L428 tumor cells share many properties such as accessory cell function, morphology, and cell surface markers with the dendritic cells described in animal and human systems.
Item Type: | Article |
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Source: | Copyright of this article belongs to American Association of Immunologists. |
ID Code: | 84800 |
Deposited On: | 27 Feb 2012 12:24 |
Last Modified: | 27 Feb 2012 12:24 |
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