Mercuric chloride‐induced anti‐glomerular basement membrane antibodies in the rat Genetic control

Druet, E; Sapin, Catherine; Günther, Eberhard; Feingold, N; Druet, Philippe

doi:10.1002/eji.1830070605

Cited by 119 publications

(47 citation statements)

References 10 publications

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“…The BN strain is known for its predisposition to develop Th2-polarized immune responses that in part might be MHC-controlled (Fournié et al 2001). Furthermore, after administration of mercury or gold salt, BN rats develop autoimmune traits that are under MHC control (Druet et al 1977;Kermarrec et al 1996). In myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), which represents a model of multiple sclerosis, the RT1 n haplotype studied here confers an early-onset, acute type, whereas other RT1 haplotypes are associated with relapsing/remitting, or mild forms.…”

Section: Rat Mhc and Disease Associationmentioning

confidence: 99%

The Genomic Sequence and Comparative Analysis of the Rat Major Histocompatibility Complex

Hurt¹,

Walter²,

Sudbrak³

et al. 2004

Genome Res.

114

106

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We have determined the sequence of a 4-Mb interval on rat chromosome 20p12 that encompasses the rat major histocompatibility complex (MHC). This is the first report of a finished sequence for a segment of the rat genome and constitutes one of the largest contiguous sequences thus far for rodent genomes in general. The rat MHC is, next to the human MHC, the second mammalian MHC sequenced to completion. Our analysis has resulted in the identification of at least 220 genes located within the sequenced interval. Although gene content and order are well conserved in the class II and class III gene intervals as well as the framework gene regions, profound rat-specific features were encountered within the class I gene regions, in comparison to human and mouse. Class I region-associated differences were found both at the structural level, the number, and organization of class I genes and gene families, and, in a more global context, in the way that evolution worked to shape the present-day rat MHC.

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Section: Rat Mhc and Disease Associationmentioning

confidence: 99%

The Genomic Sequence and Comparative Analysis of the Rat Major Histocompatibility Complex

Hurt¹,

Walter²,

Sudbrak³

et al. 2004

Genome Res.

114

106

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“…In susceptible strains of rat (17)(18)(19), subtoxic doses of mercuric chloride (HgCl2) cause immune complex glomerulopathies (17)(18)(19), often associated with autoantibodies to DNA and other anti-nuclear antigens (18,20,21). When HgC12 was administered to susceptible strains of mice, the' developed high titers of autoantibodies against nucleolar a, igens (22)(23)(24).…”

mentioning

confidence: 99%

Mercuric chloride induces autoantibodies against U3 small nuclear ribonucleoprotein in susceptible mice.

Reuter

Tessars

Vohr

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

108

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Autoantibodies to nucleolar components are a common serological feature of patients suffering from scleroderma, a collagen vascular autoimmune disease. While animal models, which spontaneously develop abundant antinucleolar antibodies, have not yet been described, high titers of such antibodies may be induced by treating susceptible strains of mice with mercuric chloride. We have identified the nucleolar autoantigen against which the HgCI2-induced IgG autoantibodies from mice of strain B10.S are directed. It is a protein with an apparent molecular mass of 36 kDa and a pI value of =8.6, which is associated with the nucleolar small nuclear RNA U3, and by these criteria must be identical with a polypeptide called fibrillarin. It is striking that scleroderma patients spontaneously produce autoantibodies against the same U3 ribonucleoprotein (RNP). The HgCl2-induced murine and the scleroderma-specific human anti-U3 RNP autoantibodies were indistinguishable in their reactivities toward fibrillarin. They further resemble each other insofar as both recognize epitopes on the 36-kDa protein, which have been highly conserved throughout evolution. Our results provide a basis to investigate at the molecular level whether similar immunoregulatory dysfunctions may lead to the preferential anti-U3 RNP autoantibody production in the animal model and in scleroderma patients.

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“…Therefore, it was of interest to compare the effects of mercury on lymphocyte subpopulations from BN, LEW, and (BN x LEW) F1 rats. The hybrids between the mercury-susceptible BN and the mercury-resistant LEW strain are susceptible to the autoimmune effects of HgCl2, a trait inherited in a dominant fashion (4). We show here that LEW rats injected with HgCI2 do not have significant decreases in RT6+ T-lymphocytes or detectable autoimmune responses.…”

mentioning

confidence: 61%

Mercury-induced renal autoimmunity: changes in RT6+ T-lymphocytes of susceptible and resistant rats.

Kosuda

Greiner

Bigazzi

1993

Environ Health Perspect

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The repeated administration of mercury to rats of the Brown Norway (BN) inbred strain results in a self-limiting production of autoantibodies to renal antigens (e.g., laminin) and autoimmune glomerulonephritis. In contrast, rats of the Lewis (LEW) strain do not develop renal autoimmunity after mercury treatment. Suppressor T-cells and/or the idiotype-anti-idiotype network have been implicated in the control of autoimmunity in susceptible (BN) rats as well as the "resistant" state of nonsusceptible (LEW) animals. In our investigations of the immune regulation of mercury-induced autoimmune glomerulonephritis, we have performed a phenotypic analysis of lymphocyte subpopulation in the spleens and lymph nodes of mercury-treated and control LEW, BN, and (BN x LEW) F1 hybrid rats. Of particular interest were RT6+ T-cells, a subpopulation of lymphocytes that may have immunoregulatory properties and show a relative decrease in mercury-treated BN rats concomitantly with the development of autoimmune responses to renal autoantigens. LEW rats did not develop renal autoimmunity after mercury treatment and had no significant change in the ratio of RT6+ to RT6- T-lymphocytes. Interestingly, the administration of mercury to (BN x LEW) F1 hybrid rats caused effects similar to those observed in the BN strain. Auto-immune responses to antigens of the kidney coincided with a change in the balance within the RT6 cell population, which was altered in favor of T-lymphocytes that do not express the RT6 phenotype.(ABSTRACT TRUNCATED AT 250 WORDS)

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Mercuric chloride‐induced anti‐glomerular basement membrane antibodies in the rat Genetic control

Cited by 119 publications

References 10 publications

The Genomic Sequence and Comparative Analysis of the Rat Major Histocompatibility Complex

The Genomic Sequence and Comparative Analysis of the Rat Major Histocompatibility Complex

Mercuric chloride induces autoantibodies against U3 small nuclear ribonucleoprotein in susceptible mice.

Mercury-induced renal autoimmunity: changes in RT6+ T-lymphocytes of susceptible and resistant rats.

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