Abstract |
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.
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Authors | H Hu, G Möller, M Abedi-Valugerdi |
Journal | Journal of autoimmunity
(J Autoimmun)
Vol. 10
Issue 5
Pg. 441-6
(Oct 1997)
ISSN: 0896-8411 [Print] England |
PMID | 9376071
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright 1997 Academic Press Limited. |
Chemical References |
- Antibodies, Monoclonal
- Cytokines
- Histocompatibility Antigens Class II
- Interleukin-2
- Interleukin-4
- Mercuric Chloride
- Interferon-gamma
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Topics |
- Animals
- Antibodies, Monoclonal
(pharmacology)
- Cell Division
(drug effects)
- Cytokines
(biosynthesis)
- Histocompatibility Antigens Class II
(physiology)
- Interferon-gamma
(biosynthesis)
- Interleukin-2
(biosynthesis)
- Interleukin-4
(biosynthesis)
- Mercuric Chloride
(antagonists & inhibitors, pharmacology)
- Mice
- Mice, Inbred BALB C
- Mice, Inbred DBA
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