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Abstract

The immune system primarily utilizes two cell types for adaptive immunity: T lymphocytes and B lymphocytes. T lymphocytes are activated when antigen presenting cells (APCs) present antigen to membrane-bound T cell receptors. B lymphocytes are activated when an antigen binds to receptors embedded in the plasma membrane. In both T and B cells this antigen binding crosslinks the receptor complexes and initiates the signal transduction cascade. These cascades frequently consist of a series of intracellular molecules becoming phosphorylated in a step-wise fashion. Once activated, these cells differentiate into effector cells that clear out the stimulating antigen. Mercury, which is a widespread environmental contaminant, is known to affect the immune system by increasing the potential for autoimmunity. The mechanisms triggered by low-level mercury exposure that cause an organism’s immune system to attack its own tissues are currently unclear. In this study, populations of EL4 T cells and WEHI-231 B cells were exposed to multiple low-level concentrations of HgCl2 for either 12 or 96 hours to mimic acute and chronic subtoxic exposure. Analytical intracellular flow cytometry was used to detect the presence of fluorescent-labeled antibodies bound to phosphorylated forms of multiple activation molecules in the signal transduction cascade. In the absence of antigenic stimulation, increased levels of activation molecules were present within both types of immune cells following low-level mercury exposure, indicating inappropriate activation of these cells by the mercury alone.

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