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Volume 272, Number 51, Issue of December 19, 1997 pp. 32411-32418

HgCl₂-induced Interleukin-4 Gene Expression in T Cells Involves a Protein Kinase C-dependent Calcium Influx through L-type Calcium Channels

(Received for publication, June 14, 1997, and in revised form, October 13, 1997)

From the INSERM Unité 28, Institut Fédératif de Recherche 30, Hôpital Purpan Place du Dr. Baylac, Toulouse 31059 cedex and ^§ CNRS, Unité Mixte de Recherche 5547, Université Paul Sabatier, Route de Narbonne, Toulouse 31062 cedex4, France

Mercuric chloride (HgCl₂) induces T helper 2 (Th2) autoreactive anti-class II T cells in Brown Norway rats. These cells produce interleukin (IL)-4 and induce a B cell polyclonal activation that is responsible for autoimmune disease. In Brown Norway rats, HgCl₂ triggers early IL-4 mRNA expression both in vivo and in vitro by T cells, which may explain why autoreactive anti-class II T cells acquire a Th2 phenotype. The aim of this study was to explore the transduction pathways by which this chemical operates. By using two murine T cell hybridomas that express IL-4 mRNA upon stimulation with HgCl₂, we demonstrate that: 1) HgCl₂ acts at the transcriptional level without requiring de novo protein synthesis; 2) HgCl₂ induces a protein kinase C-dependent Ca²⁺ influx through L-type calcium channels; 3) calcium/calcineurin-dependent pathway and protein kinase C activation are both implicated in HgCl₂-induced IL-4 gene expression; and 4) HgCl₂ can activate directly protein kinase C, which might be one of the main intracellular target for HgCl₂. These data are in agreement with an effect of HgCl₂ which is independent of antigen-specific recognition. It may explain the T cell polyclonal activation in the mercury model and the expansion of pathogenic autoreactive anti-class II Th2 cells in this context.

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