Immunological Studies on the Mechanism of Gold Hypersensitivity Reactions

P, Davis; Ezeoke, A. C. J.; Munro, Janet; Hobbs, J. R.; Hughes, G. R. V.

doi:10.1136/bmj.3.5882.676

Cited by 55 publications

(17 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Second, chemicals known to induce allergic reactions might protect from TH1-mediated autoimmune disorders. In that respect it is interesting to note that gold salts which have beneficial effects on rheumatoid arthritis are also able to induce an increase in serum IgE concentration and/or autoimmunity [44,45] in susceptible individuals and a THZmediated disease in BN rats quite similar to that induced by HgC12 [46]. Furthermore we recently showed that gold salts also prevent development of EAU in F1 rats (unpublished).…”

Section: Discussionmentioning

confidence: 93%

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

et al. 1993

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 93%

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

et al. 1993

View full text Add to dashboard Cite

show abstract

“…The reason for these different kinet ics is not known. Increased levels of total serum IgE were also found in patients treated with GST [31 ].…”

Section: Discussionmentioning

confidence: 67%

Immunological Alterations Inducible by Mercury Compounds

Pietsch

Vohr

Degitz

et al. 1989

Int Arch Allergy Immunol

View full text Add to dashboard Cite

We determined the levels of total IgE, IgG and IgM in the sera of HgCl₂ and gold sodium thiomalate (GST) treated A.SW, C57Bl/6, and DBA/2 mice. In HgCl₂ treated A.SW mice, IgE and IgG levels increased up to 30 times above normal. In C57Bl/6 mice HgCl₂ induced a slight IgE increase, but no change in IgG. Strain DBA/2, by contrast, did not show significant increases in either IgE or IgG. A.SW mice also proved susceptible to the immunostimulatory effects of GST in that they responded by significant increases in IgE, IgG, and IgM. C57Bl/6 mice responded to GST by an increase in IgM alone, and DBA/2 mice again, were resistant. The same strain-specific responses have been reported with respect to the autoimmunizing effects inducible by HgCl₂ and GST.

show abstract

“…Allergic reaction to gold salts might have been responsible for the development of this nephritis. However, such immunological phenomena are rarely seen in the patients with gold-induced nephropathy [50,51]. Furtherrnore, to date, no evidence for the presence of gold in renal immune deposits has been reported.…”

Section: Pathogenesismentioning

confidence: 94%

“…To clarify the pathogenesis of this nephropathy, it is ,necessary to confirrn the specificity of the antigens and antibodies responsible for the immune complex of the glomerular lesions. Gold salts may be able to act as a hapten, and specific IgE antibodies against gold salts have been detected in the sera of rheumatoid arthritis patients with some mucocutaneous and hematologic adverse re action to gold salts [50,51]. A positive lymphocyte transformation test to gold salts is also seen in some rheumatoid arthritis patients with hematologic side effects after chrysotherapy [52].…”

Section: Pathogenesismentioning

confidence: 96%

Nephrotoxicity of gold salts, D-penicillamine, and allopurinol

Ueda¹

1998

Clinical Nephrotoxins

View full text Add to dashboard Cite

Immunological Studies on the Mechanism of Gold Hypersensitivity Reactions

Cited by 55 publications

References 7 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

Immunological Alterations Inducible by Mercury Compounds

Nephrotoxicity of gold salts, D-penicillamine, and allopurinol

Contact Info

Product

Resources

About