DESIALYLATION OF T-LYMPHOCYTES OVERCOMES THE MONOCYTE DEPENDENCY OF POKEWEED MITOGEN-INDUCED T-CELL ACTIVATION

Citation
T. Gallart et al., DESIALYLATION OF T-LYMPHOCYTES OVERCOMES THE MONOCYTE DEPENDENCY OF POKEWEED MITOGEN-INDUCED T-CELL ACTIVATION, Immunology, 90(1), 1997, pp. 57-65
Citations number
32
Categorie Soggetti
Immunology
Journal title
ISSN journal
00192805
Volume
90
Issue
1
Year of publication
1997
Pages
57 - 65
Database
ISI
SICI code
0019-2805(1997)90:1<57:DOTOTM>2.0.ZU;2-J
Abstract
Activation of T lymphocytes by pokeweed mitogen (PWM) is strictly mono cyte (Mo)-dependent and results in T-cell mitogenesis and interleukin- 2 (IL-2) secretion, coupled with an inability to utilize IL-2 due to a n impaired expression of functional IL-2 receptor (IL-2R). Such IL-2R impairment could arise in PWM-activated T cells themselves or, alterna tively, be the result of Mo-derived influences, as it is known that PW M binds Mo strongly and does not or poorly binds lymphocytes, and Mo b ecomes rapidly destroyed in PWM-stimulated cultures of blood mononucle ar cells or T cells plus Mo. The present study investigated these poss ibilities. The results show for the first time that desialylation of T lymphocytes strongly increases their PWM-binding capacity and, in add ition, overcomes the Mo requirement for PWM to induce T-cell mitogenes is and IL-2 secretion. Such secreted IL-2 levels were even higher that those found in cultures of Mo-dependent PWM-activated T lymphocytes b ut, similarly to the latter, PWM-activated desialylated purified T lym phocytes exhibited negligible high-affinity IL-2 binding capacity and an inability to utilize the IL-2 they produced. These effects were not due to desialylation itself, as indicated by data obtained with peanu t agglutinin, a lectin that becomes strongly reactive with desialylate d T lymphocytes. The data clearly indicate the existence of PWM-relate d events capable of impairing the expression of functional IL-2R witho ut affecting IL-2 secretion, and indicate that such events are due to mechanisms arising at the level of PWM-activated T cells themselves.