Major histocompatibility complex class II antigens are required for both cytokine production and proliferation induced by mercuric chloride in vitro

• Published in: Journal of autoimmunity 1997-10, Vol.10 (5), p.441-446
• Main Authors: HU, H, MÖLLER, G, ABEDI-VALUGERDI, M
• Format: Article
• Language: English
• Subjects: Animals; Antibodies, Monoclonal - pharmacology; Biological and medical sciences; Cell Division - drug effects; Cytokines - biosynthesis; Experimental and animal immunopathology. Animal models; Histocompatibility Antigens Class II - physiology; Immunopathology; Interferon-gamma - biosynthesis; Interleukin-2 - biosynthesis; Interleukin-4 - biosynthesis; Medical sciences; Mercuric Chloride - antagonists & inhibitors; Mercuric Chloride - pharmacology; Mice; Mice, Inbred BALB C; Mice, Inbred DBA
• ISSN: 0896-8411; 1095-9157
• DOI: 10.1006/jaut.1997.9997

Autoimmune diseases induced by mercuric chloride are genetically determined, at least one gene being major histocompatibility complex (MHC)-linked. Previously, we showed that in vitro mercury stimulation induced a high proliferative response in lymphocytes from susceptible mice (high-responders) and that the proliferative response could be restored in lymphocytes from low-responders by pretreating the cells with mercury. We also found that the continuous presence of mercury induced IL-2 and IFN-gamma production, while pretreatment with mercury induced IL-4 production. In this study, we showed that anti-MHC class II monoclonal antibodies blocked both the mercury-induced proliferative responses in lymphocytes from high-responders and the restored proliferative responses in low-responders. In addition, anti-MHC class II antibodies also inhibited the mercury-induced IL-2, IFN-gamma and IL-4 cytokine production in vitro. The results demonstrate that MHC class II antigens directly participate in mercury-induced cytokine production and cell activation, and are required at the onset of the initiation.