Animal models of autoimmune thyroiditis: recent advances

Kong, Yi‐chi M.

doi:10.1007/978-94-011-5044-6_1

Cited by 2 publications

(4 citation statements)

References 96 publications

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“…Current Protocols in Immunology in thyroid infiltration by adoptive transfer into unimmunized mice (Kong, 1998). As a normally circulating self antigen, MTg is usually nonimmunogenic.…”

Section: Supplement 78mentioning

confidence: 99%

“…Similar studies have shown that the participation of iodine residues on algorithm‐predicted T cell epitopes in pathogenicity depends on the amino acid composition (Li et al, ). Other examples include determining the pathologic participation of Vβ13 + , but not Vβ8 + T cells, in thyroid infiltration by adoptive transfer into unimmunized mice (Kong, ).…”

Section: Commentarymentioning

confidence: 99%

“…Hashimoto's thyroiditis (HT) and mouse thyroglobulin (MTg)-induced EAT share the persistent characteristics of mononuclear cell infiltration, follicular destruction, autoantibody production, and T cell proliferative response to thyroglobulin (Tg). As reviewed recently (Kong, 1998;Morris and Kong, 2006), studies of EAT have provided insights into cellular infiltration kinetics (the role of T cell subsets and macrophages), short-and long-term effects of immunotherapy, involvement of cytotoxic T cells, and the role of regulatory T cells in preventing EAT induction.…”

Section: Commentary Background Informationmentioning

confidence: 99%

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Experimental Autoimmune Thyroiditis in the Mouse

Kong

2007

CP in Immunology

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Experimental autoimmune thyroiditis (EAT) in mice is an excellent model for Hashimoto's thyroiditis (HT). It is induced with thyroglobulin (Tg), a known thyroid autoantigen that is common to both mouse and human and for which several conserved, thyroiditogenic epitopes have been identified. This unit describes induction and evaluation of EAT using thyroid histology and in vitro proliferative response assays. An ELISA is presented to detect the level of antibody to mouse thyroglobulin (MTg). To induce EAT, either bacterial lipopolysaccharide (LPS) or supplemented complete Freund's adjuvant (CFA) can be used as adjuvant. A support protocol for preparing MTg is included. The T cell proliferation assay can be used to examine the antigenicity of synthetic peptides derived from MTg or heterologous Tg. EAT can be adoptively transferred utilizing cells that have been expanded in vitro, as described. A protocol is provided for inducing tolerance using deaggregated MTg; induction of tolerance requires larger amounts of MTg but efficiently suppresses EAT development. Also included is a protocol to demonstrate the role of regulatory T cells in mediating tolerance. A protocol to delineate HLA association with HT is illustrated using HLA class II transgenic mice.

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“…Current Protocols in Immunology in thyroid infiltration by adoptive transfer into unimmunized mice (Kong, 1998). As a normally circulating self antigen, MTg is usually nonimmunogenic.…”

Section: Supplement 78mentioning

confidence: 99%

Section: Commentarymentioning

confidence: 99%

Section: Commentary Background Informationmentioning

confidence: 99%

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Experimental Autoimmune Thyroiditis in the Mouse

Kong

2007

CP in Immunology

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“…The evidence is clear in the NOD mouse with EAT‐susceptible alleles; treatment of NOD ( IA g7 ) and NOD.H2 h4 ( IA k ) mice with sodium iodide (NaI, 0·05%) in the drinking water for 4–8 weeks resulted in an increase in thyroiditis incidence [9–11]. Epidemiological surveys in humans, however, show that the extent of influence of iodine intake is less clear and is highly dependent on genetic/ethnic differences and less on dietary customs [12–14].…”

Section: Introductionmentioning

confidence: 99%

Depletion of CD4+CD25+ regulatory T cells exacerbates sodium iodide-induced experimental autoimmune thyroiditis in human leucocyte antigen DR3 (DRB1*0301) transgenic class II-knock-out non-obese diabetic mice

Flynn

Meroueh

Snower

et al. 2007

Clinical and Experimental Immunology

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Both genetic and environmental factors contribute to autoimmune disease development. Previously, we evaluated genetic factors in a humanized mouse model of Hashimoto's thyroiditis (HT) by immunizing human leucocyte antigen DR3 (HLA-DR3) and HLA-DQ8 transgenic class II-knock-out non-obese diabetic (NOD) mice. DR3+ mice were susceptible to experimental autoimmune thyroiditis (EAT) induction by both mouse thyroglobulin (mTg) and human (h) Tg, while DQ8+ mice were weakly susceptible only to hTg. As one environmental factor associated with HT and tested in non-transgenic models is increased sodium iodide (NaI) intake, we examined the susceptibility of DR3+ and/or DQ8+ mice to NaI-induced disease. Mice were treated for 8 weeks with NaI in the drinking water. At 0 x 05% NaI, 23% of DR3+, 0% of DQ8+ and 20% of DR3+DQ8+ mice had thyroid destruction. No spleen cell proliferation to mTg was observed. Most mice had undetectable anti-mTg antibodies, but those with low antibody levels usually had thyroiditis. At 0.3% NaI, a higher percentage of DR3+ and DR3+DQ8+ mice developed destructive thyroiditis, but it was not statistically significant. However, when DR3+ mice had been depleted of CD4+CD25+ regulatory T cells prior to NaI treatment, destructive thyroiditis (68%) and serum anti-mTg antibodies were exacerbated further. The presence of DQ8 molecules does not alter the susceptibility of DR3+DQ8+ mice to NaI-induced thyroiditis, similar to earlier findings with mTg-induced EAT. Susceptibility of DR3+ mice to NaI-induced EAT, in both the presence and absence of regulatory T cells, demonstrates the usefulness of HLA class II transgenic mice in evaluating the roles of environmental factors and immune dysregulation in autoimmune thyroid disease.

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Animal models of autoimmune thyroiditis: recent advances

Cited by 2 publications

References 96 publications

Experimental Autoimmune Thyroiditis in the Mouse

Experimental Autoimmune Thyroiditis in the Mouse

Depletion of CD4+CD25+ regulatory T cells exacerbates sodium iodide-induced experimental autoimmune thyroiditis in human leucocyte antigen DR3 (DRB1*0301) transgenic class II-knock-out non-obese diabetic mice

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