Inhibition of experimental autoimmune uveoretinitis by mercuric chloride injections in (Lewis X Brown Norway) F1 hybrid rats

Saoudi, Abdelhadi; Bellon, B; Kozak, Y. de; Vial, M C; Thillaye, B.; Druet, Philippe

doi:10.3109/02713689008999433

Cited by 6 publications

(7 citation statements)

References 6 publications

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“…As previously described we observed that (LEW X BN) F1 rats immunized with S-Ag seven days after the first injection of HgC12 were protected from EAU [30]. We now show that this protection is associated with a drastically decreased ability of LN cells to transfer EAU.…”

Section: Discussionsupporting

confidence: 63%

“…Effect of HgC12 on active EAU in (LEW X BN) F1 rats injected with 1.5 x lo8 cells from H2O S-Ag rats ( Table 2). As already observed [30], LN cells from protected rats as well as those from diseased rats (data not shown) proliferated in vitro in the presence of S-Ag. were measured in supernatants using biological assays (see Sect.…”

Section: Lymph Node Cells From Protected Rats Fail To Transfer Eaumentioning

confidence: 51%

“…As previously described [30], (LEW X BN) F1 rats injected with HgC12 for 7 days and then immunized with S-Ag were protected from EAU (Table 1). In the experiment presently reported, none of the five HgCl2-injected rats developed EAU while the five rats injected with the control solution exhibited a severe clinical and histological EAU.…”

Section: Hgclz-injected Rats Are Protected From Active Eaumentioning

confidence: 91%

“…Experiments are in progress to derive such T cell lines. That immunization with S-Ag on day 14 [30] or 21 (not shown) after the first HgC12 injection was less or not efficient was expected.…”

Section: Discussionmentioning

confidence: 99%

“…We previously demonstrated that (LEW X BN) F1 rats immunized with S-Ag 7 days after the first HgC12 injection were protected against EAU [30]. Lymph node [LN] cells from protected rats proliferated as well as those from diseased rats in the presence of S-Ag and the anti-S-Ag antibody titer was similar in both groups [30]. Activated LN cells from (LEW X BN) F1 rats immunized with S-Ag were able to transfer EAU into (LEW X BN) F1 rats injected with HgCl2 [31].…”

Section: Introductionmentioning

confidence: 99%

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TH2 activated cells prevent experimental autoimmune uveoretinitis, a TH1‐dependent autoimmune disease

et al. 1993

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Mercuric chloride (HgCl2) injections protect (Lewis x Brown-Norway) F1 (F1) rats against experimental autoimmune uveoretinitis (EAU) induced by immunization with the retinal S antigen (S-Ag); in contrast HgCl2-injected F1 rats develop EAU following transfer of lymph node (LN) cells from rats immunized with S-Ag alone. In the present study we demonstrate that the ability of LN cells from rats protected against EAU to transfer the disease into naive F1 rats was considerably reduced. These LN cells neither produced interleukin (IL)-2 nor (interferon (IFN)-gamma but exhibited mRNA for IL-4. In contrast, LN cells from diseased rats easily transferred EAU into naive F1 rats, produced significant IL-2 and IFN-gamma levels but barely exhibited mRNA for IL-4. Furthermore protected rats predominantly produced IgG1 anti-S-Ag antibodies, while diseased rats produced IgG2b anti-S-Ag antibodies and the increase in expression of MHC class II molecules on B cells was higher in protected rats than in diseased rats. These data suggest that (1) to exert a protective effect, HgCl2 must act at an early stage of differentiation of precursors of S-Ag specific T cells, and (2) this effect is related to the preferential activation of TH2 cells to the detriment of uveitogenic TH1 cells. Finally, these results indicate that activation of TH2 cells protect from a TH1-dependent autoimmune disease.

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Section: Discussionsupporting

confidence: 63%

Section: Lymph Node Cells From Protected Rats Fail To Transfer Eaumentioning

confidence: 51%

Section: Hgclz-injected Rats Are Protected From Active Eaumentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

TH2 activated cells prevent experimental autoimmune uveoretinitis, a TH1‐dependent autoimmune disease

et al. 1993

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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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Mercury enhances susceptibility to murine leishmaniasis

Bagenstose

Mentink‐Kane

Brittingham

et al. 2001

Parasite Immunology

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The genetic background of mice infected with Leishmania major determines the response to infection, resulting in a resistant or susceptible phenotype. Susceptible mice develop a T-helper type 2 (Th2)-type immune response following infection distinguished by the development of interleukin (IL)-4 secreting T cells in the lymph node and spleen. In SJL mice, which normally heal L. major lesions, subtoxic doses of mercury induce an autoimmune syndrome characterized by an expansion of Th2 cells. In this study, we examined the effect of mercury administration on the outcome of L. major infection in SJL mice. We show that subtoxic doses of mercuric chloride (HgCl2) exacerbate disease outcome in SJL mice resulting in increased footpad swelling and increased parasite burdens. Furthermore, the effects of HgCl2 treatment on resistance to L. major are time-dependent. The nonhealing phenotype was observed only if mice had been treated with HgCl2 prior to L. major infection for at least 1 week, a timepoint at which mice treated with HgCl2 alone had increased splenocyte IL-4 production. HgCl2 treatment also increased production of serum immunoglobulin (Ig)E and IgG1, two IL-4 dependent isotypes. These results show that HgCl2 treatment enhances the susceptibility to L. major in SJL mice, consistent with the induction of host Th2 parameters. These findings have implications for the role of mercury contamination in areas of endemic leishmaniasis.

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Inhibition of experimental autoimmune uveoretinitis by mercuric chloride injections in (Lewis X Brown Norway) F1 hybrid rats

Cited by 6 publications

References 6 publications

TH2 activated cells prevent experimental autoimmune uveoretinitis, a TH1‐dependent autoimmune disease

TH2 activated cells prevent experimental autoimmune uveoretinitis, a TH1‐dependent autoimmune disease

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

Mercury enhances susceptibility to murine leishmaniasis

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