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Desialylation of T lymphocytes overcomes the monocyte dependency of pokeweed mitogen‐induced T‐cell activation
Author(s) -
GALLART T.,
ANGEL DE LA FUENTE M.,
JOSEP BARCELÓ J.,
ALBEROLAILA J.
Publication year - 1997
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1997.00129.x
Subject(s) - pokeweed mitogen , monocyte , dependency (uml) , immunology , lymphocyte activation , t cell , biology , microbiology and biotechnology , genetics , immune system , computer science , concanavalin a , in vitro , software engineering
Activation of T lymphocytes by pokeweed mitogen (PWM) is strictly monocyte (Mo)‐dependent and results in T‐cell mitogenesis and interleukin‐2 (IL‐2) secretion, coupled with an inability to utilize IL‐2 due to an impaired expression of functional IL‐2 receptor (IL‐2R). Such IL‐2R impairment could arise in PWM‐activated T cells themselves or, alternatively, be the result of Mo‐derived influences, as it is known that PWM binds Mo strongly and does not or poorly binds lymphocytes, and Mo becomes rapidly destroyed in PWM‐stimulated cultures of blood mononuclear cells or T cells plus Mo. The present study investigated these possibilities. The results show for the first time that desialylation of T lymphocytes strongly increases their PWM‐binding capacity and, in addition, overcomes the Mo requirement for PWM to induce T‐cell mitogenesis and IL‐2 secretion. Such secreted IL‐2 levels were even higher that those found in cultures of Mo‐dependent PWM‐activated T lymphocytes but, similarly to the latter, PWM‐activated desialylated purified T lymphocytes 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 peanut agglutinin, a lectin that becomes strongly reactive with desialylated T lymphocytes. The data clearly indicate the existence of PWM‐related events capable of impairing the expression of functional IL‐2R without affecting IL‐2 secretion, and indicate that such events are due to mechanisms arising at the level of PWM‐activated T cells themselves.