Effect of HgCl2 on experimental allergic encephalomyelitis in Lewis rats. HgC12i-nduced down-modulation of the disease

Pelletier, Lucette; Rossert, Jérôme; Pasquier, R. Du; Villarroya, H.; Bélair, Marie‐France; Vial, M C; Oriol, Rafaël; Druet, Philippe

doi:10.1002/eji.1830180210

Cited by 35 publications

(17 citation statements)

References 25 publications

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“…Contact allergic reactions to dental amalgam are found in a minority of the population (%lo), but there are several reports in animal and in vitro studies on the effects of mercury on the immune system. Thus, mercury chloride may cause non-specific immu-nosuppression (11,12) and proliferation of T and B cells (13), which may induce formation of polyclonal activation of the B lymphocytes, requiring T cells (14)(15)(16). Mercury salts may also induce antinuclear antibodies (14)(15)(16)(17)(18)(19), anti-glomerular basement membrane antibodies, and anti-DNA antibodies (16,(20)(21)(22), increases of serum IgE (15,16,23) and immune complexes (16,(20)(21)(22), and activation of the coagulation system (24).…”

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confidence: 99%

Comprehensive medical examination of a group of patients with alleged adverse effects from dental amalgams

Anneroth

Ericson

Johansson

et al. 1992

Acta Odontologica Scandinavica

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Mercury from dental amalgams does not seem to cause dose-related intoxications. However, animal studies have shown that high-dose exposure to mercury may support various types of immunologic reactions. Ten patients claiming that their symptoms were caused and aggravated by amalgam therapy were selected for a study of the effects of removal of one amalgam restoration followed by placing of a composite filling. Clinical symptoms and the result of laboratory tests were recorded. Six patients had contact allergies to metals, three of them to mercury ammonium chloride. The comparison of pre- and post-experimental test results showed significant reductions in p-IgE and dU-albumin and significant increases in p-C3d and dU-beta 2-microglobulin. There was no laboratory evidence of a direct toxic effect by mercury on the patients. The observed response by some of the studied factors to the low acute exposure to amalgam may imply that an activation of the immune system occurred.

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confidence: 99%

Comprehensive medical examination of a group of patients with alleged adverse effects from dental amalgams

Anneroth

Ericson

Johansson

et al. 1992

Acta Odontologica Scandinavica

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“…This immunosuppression is mediated by non-antigen-specific CD8 + cells responsible for depression of T cell functions (4). HgCl2-injected LEW rats are protected against Heymann's nephritis (5) and experimental autoimmune encephalomyelitis (EAE) (6,7). Protection is I Abbreviations used in this paper: BN, Brown-Norway; BP, myelin basic protein; EAE, experimental autoimmune encephalomyelitis; LDA, limiting dilution analysis; LEW, Lewis; PPD, purified protein derivative.…”

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Mercury-induced autoreactive anti-class II T cell line protects from experimental autoimmune encephalomyelitis by the bias of CD8+ antiergotypic cells in Lewis rats.

Castedo

Pelletier

Rossert

et al. 1993

The Journal of Experimental Medicine

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SummaryBrown-Norway (BN) rats injected with HgC12 develop a systemic autoimmune disease associated with a polyclonal B cell activation, due to autoreactive T cells specific for self-class II molecules, while Lewis (LEW) rats injected with HgCI2 do not exhibit autoimmunity and develop a non-antigen-specific, CD8-mediated immunosuppression assessed by a depression of T cell functions, and a protection against experimental autoimmune encephalomyelitis (EAE). Resistance to HgC12-induced autoimmunity is not due to these suppressor cells since treatment with an anti-CD8 monoclonal antibody (mAb) did not allow autoimmunity to appear. The absence of autoimmunity in this strain could result from the absence of autoreactive T cells, or from quantitative or qualitative differences of these cells between susceptible and resistant strains. In the present study, we show that CD4 + anti-class IIT ceils are present in HgC12-injected LEW rats and are as frequent as in BN rats when assessed by limiting dilution analysis. LEW CD4 + autoreactive T cell lines were derived. They proliferated in the presence of normal class II-bearing cells, secreted interleukin 2, and did not induce B cells to produce immunoglobulins. Transfer of one of these lines, LEW Hg A, into normal LEW rats led to the appearance of CD8 + cells responsible for a non-antigen-specific immunosuppression that induced complete protection from EAE. Immunosuppression was abrogated after treatment with an anti-CD8 mAb. In vitro, CD8 + ceUs from rats injected with the LEW Hg A T cell line proliferated in the presence of activated T cells whatever their origin. We conclude that HgC12 induces CD4 + autoreactive T cells that proliferate in the presence of class II + cells in susceptible BN as well as in resistant LEW rats. But while these cells collaborate with B ceils to produce autoantibodies in BN rats, they initiate in LEW rats a suppressor circuit involving antiergotypic CD8 + suppressor cells. Brown-Norway (BN) 1 rats injected with HgC12 develop lupus-like systemic autoimmune disease in the context of a polyclonal B cell activation (1, 2), due to autoreactive T cells specific for self-class II molecules (3). In contrast, Lewis (LEW) rats injected with HgC12 do not develop autoimmunity but exhibit a non-antigen specific CD8-mediated immunosuppression (4). This immunosuppression is mediated by non-antigen-specific CD8 + cells responsible for depression of T cell functions (4). HgCl2-injected LEW rats are protected against Heymann's nephritis (5) and experimental autoimmune encephalomyelitis (EAE) (6, 7). Protection is I Abbreviations used in this paper: BN, Brown-Norway; BP, myelin basic protein; EAE, experimental autoimmune encephalomyelitis; LDA, limiting dilution analysis; LEW, Lewis; PPD, purified protein derivative. not absolute, probably due to the emergence of contrasuppressor ceils (7). Until now, the way these suppressor cells were induced and their specificity were unknown. Since anti-class IIT cells were present in BN rats injected with HgCI2 (3) and since in...

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“…In fact, beneficial effects of mercury have also been demonstrated in several other experimental autoimmune models. For instance, chronic injection with mercury could protect the Lewis rats against Heymann's nephritis [36] and experimental autoimmune encephalomyelitis (EAE) [37]. Treatment with mercury could also prevent the experimental autoimmune uveoretinitis (EAU) and pinealitis (EAP) in (Lewis × Brown‐Norway) F1 rats [38].…”

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confidence: 99%

Analysis of mercury-induced immune activation in nonobese diabetic (NOD) mice

Brenden¹,

Rabbani

Abedi‐Valugerdi

2001

Clinical and Experimental Immunology

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In susceptible mice, the heavy metal ion mercury is able to induce a strong immune activation, which resembles a T helper 2 (Th2) type of immune response and is characterized by a polyclonal B cell activation, formation of high levels of IgG1 and IgE antibodies, production of autoantibodies of different specificities and development of renal IgG deposits. In the present study, we analysed the in vivo effects of mercury in nonobese diabetic (NOD) mice, which is believed to develop a spontaneous Th1 cell-mediated autoimmune diabetes similar to type 1 diabetes in humans. Three weeks of treatment with mercury induced a strong Th2 like immune/autoimmune response in NOD mice. This response was characterized by an intensive increase in splenic IgG1 antibody secreting cells, a marked elevation in serum IgE levels, a substantial increase in splenic IL-4 mRNA, but a significant decrease in splenic IFN-gamma mRNA. Mercury-induced IgG1 antibodies were mainly against ssDNA, TNP and thyroglobulin, but not against nucleolar antigen. Moreover, mercury-injected NOD mice developed high titres of IgG1 deposits in the kidney glomeruli. We further tested if the generated Th2 response could interfere with the development of insulitis and diabetes in NOD mice. We found that three weeks of treatment with mercury was also able to significantly suppress the development of insulitis and postpone the onset of diabetes in these mice. Thus, mercury-induced immune activation can counter-regulate the Th1 cell-mediated autoimmune responses and confer a partial protection against autoimmune diabetes in NOD mice.

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Effect of HgCl2 on experimental allergic encephalomyelitis in Lewis rats. HgC12i-nduced down-modulation of the disease

Cited by 35 publications

References 25 publications

Comprehensive medical examination of a group of patients with alleged adverse effects from dental amalgams

Comprehensive medical examination of a group of patients with alleged adverse effects from dental amalgams

Mercury-induced autoreactive anti-class II T cell line protects from experimental autoimmune encephalomyelitis by the bias of CD8+ antiergotypic cells in Lewis rats.

Analysis of mercury-induced immune activation in nonobese diabetic (NOD) mice

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