Effect of guinea pig thyroglobulin in incomplete Freund's adjuvant on experimental autoimmune thyroiditis induced by in vitro-activated lymph node cells

1983 ◽  
Vol 76 (1) ◽  
pp. 113-119 ◽  
Author(s):  
Helen Braley-Mullen ◽  
Julia G. Tompson ◽  
Gordon C. Sharp ◽  
Michael Kyriakos
Keyword(s):  
Lymph Node ◽  
Guinea Pig ◽  
Autoimmune Thyroiditis ◽  
Experimental Autoimmune Thyroiditis ◽  
Incomplete Freund’S Adjuvant ◽  
Lymph Node Cells ◽  
Freund’S Adjuvant ◽  
Freund's Adjuvant ◽  
Experimental Autoimmune

scholarly journals A thyroxine-containing peptide can induce murine experimental autoimmune thyroiditis.

1992 ◽  
Vol 175 (3) ◽  
pp. 869-872 ◽  
Author(s):  
P R Hutchings ◽  
A Cooke ◽  
K Dawe ◽  
B R Champion ◽  
M Geysen ◽  
...  
Keyword(s):  
Lymph Node ◽  
T Cell ◽  
Autoimmune Thyroiditis ◽  
Synthetic Peptide ◽  
Experimental Autoimmune Thyroiditis ◽  
Intact Mouse ◽  
Autoreactive T Cell ◽  
Lymph Node Cells ◽  
Experimental Autoimmune

A synthetic peptide based on a sequence containing thyroxine at position 2553 in thyroglobulin (Tg), and already shown to be recognized by two clonotypically distinct murine Tg autoreactive T cell hybridomas, can trigger primed lymph node cells to transfer thyroiditis to naive recipients. Donor lymph node cells could be prepared from mice immunized either with intact mouse Tg or with this peptide itself. After a second exposure to the priming antigen in vitro, both these populations induced 100% thyroiditis in recipient animals. The importance of the T4 residue in the development of disease was demonstrated by the failure of Tg tryptic peptides depleted of T4 to stimulate pathogenic effectors in vitro, even when the lymph node cells had been taken from mice primed with whole Tg. We conclude that this T4-containing 12mer sequence is a major thyroiditogenic epitope in CBA/J mice although we cannot exclude the possibility that there are other pathogenic epitopes present in the whole Tg molecule.

scholarly journals Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Inhibits Experimental Autoimmune Thyroiditis by the Expansion of CD4+CD25+ Regulatory T Cells

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 2000-2007 ◽  
Author(s):  
Su He Wang ◽  
Gwo-Hsiao Chen ◽  
Yongyi Fan ◽  
Mary Van Antwerp ◽  
James R. Baker
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Autoimmune Thyroiditis ◽  
Rabbit Model ◽  
Experimental Autoimmune Thyroiditis ◽  
Autoimmune Encephalomyelitis ◽  
Necrosis Factor ◽  
Experimental Autoimmune

There have been several reports that TNF-related apoptosis-inducing ligand (TRAIL) has the ability to suppress the development of experimental autoimmune diseases, including a mouse model of experimental autoimmune encephalomyelitis, a rabbit model of rheumatoid arthritis, type 1 diabetes mellitus, in mice and experimental autoimmune thyroiditis (EAT) in mice. However, the mechanism underlying TRAIL effect is not well defined. In the present study, we specifically examined TRAIL effects on CD4+CD25+ regulatory T cells. CD4+CD25+ T cells prepared from mouse thyroglobulin (mTg)-immunized CBA/J mice proliferate in the presence of TRAIL and dendritic cells in vitro. These CD4+CD25+ T cells included both CD4+CD25+CD45RBLow (regulatory) and CD4+CD25+CD45RBHigh (effector) T cells. Our results demonstrated that mTg-immunized mice treated with TRAIL showed significant increases in the number of CD4+CD25+CD45RBLow T cells compared with mice immunized with mTg alone. CD4+CD25+CD45RBLow T cells expressed much higher levels of the forkhead family transcription factor, IL-10, and TGFβ1 than CD4+CD25+CD45RBHigh T cells, and these cells can completely suppress the proliferation of the mTg-primed splenocytes in lower concentrations than the unfractionated CD4+CD25+ T cells. Furthermore, transfer of these cells into CBA/J mice prior to mTg-primed splenocyte injection could markedly reduce the frequency and severity of EAT development. CD4+CD25+CD45RBLow T cells were more effective at suppressing histological thyroiditis than unfractionated cells. These results indicated that TRAIL can increase the number of mTg-specific CD4+CD25+CD45RBLow T cells, inhibiting autoimmune responses and preventing the progression of EAT. These findings reveal a novel mechanism by which TRAIL could inhibit autoimmune disease.

scholarly journals Cultured Murine Thyroid Epithelial Cells Expressing Transgenic Fas-Associated Death Domain-Like Interleukin-1β Converting Enzyme Inhibitory Protein Are Protected from Fas-Mediated Apoptosis

Endocrinology ◽  
2008 ◽  
Vol 149 (7) ◽  
pp. 3321-3329 ◽  
Author(s):  
Yujiang Fang ◽  
Helen Braley-Mullen
Keyword(s):  
Epithelial Cells ◽  
Autoimmune Thyroiditis ◽  
Death Domain ◽  
Converting Enzyme ◽  
Experimental Autoimmune Thyroiditis ◽  
Inhibitory Protein ◽  
Rna Transfection ◽  
Experimental Autoimmune

The antiapoptotic molecule Fas-associated death domain-like IL-1β-converting enzyme inhibitory protein (FLIP) inhibits Fas-mediated apoptosis by blocking activation of caspase-8. We previously showed that expression of transgenic FLIP on thyroid epithelial cells (TECs) of DBA/1 and CBA/J mice promoted earlier resolution of granulomatous experimental autoimmune thyroiditis in vivo. This study was undertaken to directly determine whether transgenic FLIP expressed on cultured TECs can protect TECs from Fas-mediated apoptosis in vitro. The results indicate that cultured TECs from DBA/1 and CBA/J mice can be sensitized in vitro by interferon-γ and TNF-α to undergo Fas-mediated apoptosis. Transgenic overexpression of FLIP protected cultured TECs of FLIP transgene (Tg)+ DBA/1 and CBA/J mice from Fas-mediated apoptosis, and FLIP small interfering RNA transfection of cultured TECs of FLIP Tg+ DBA/1 and CBA/J mice abolished the protective effect. These in vitro results are consistent with our previous in vivo studies using DBA/1 and CBA/J FLIP Tg+ mice and provide direct support for the hypothesis that transgenic expression of FLIP promotes resolution of granulomatous experimental autoimmune thyroiditis by protecting TECs from apoptosis.

scholarly journals Iodine Intake Increases IP-10 Expression in the Serum and Thyroids of Rats with Experimental Autoimmune Thyroiditis

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Si-lu Cui ◽  
Jun Yu ◽  
Liu Shoujun
Keyword(s):  
Autoimmune Thyroiditis ◽  
Thyroid Tissue ◽  
Iodine Concentration ◽  
Iodine Intake ◽  
Experimental Autoimmune Thyroiditis ◽  
High Iodine ◽  
Incomplete Freund’S Adjuvant ◽  
Iodine Treatment ◽  
Inducible Protein ◽  
Experimental Autoimmune

Here, we sought to establish an experimental autoimmune thyroiditis rat model induced by bovine thyroglobulin (bTg) injection and to investigate pathological changes and variations in serum interferon-γ-inducible protein of 10 kDa (IP-10) in thyroid tissue following iodine treatment. Four-week-old female Lewis rats(n=135)were randomly divided into normal (NC), thyroglobulin (TG), HI, HI+TG, HII, and HII+TG groups; rats in the NC and TG groups drank only distilled water (iodine concentration: 10 μg/L), rats in the HI and HI+TG groups were given water containing 25.7 mg/L iodine, and rats in the HII and HII+TG groups were given water containing 423.3 mg/L iodine. Rats in the TG, HI+TG, and HII+TG groups were immunized with 0.1 mL bTg (8 mg/mL) in incomplete Freund’s adjuvant once every 2 weeks for 6 weeks. Compared with the NC group, the TG, HI+TG, and HII+TG groups exhibited higher iodine intake and increased thyroid weights with increasing iodine doses(P<0.05). The high iodine intake in the TG group was associated with increased CD4+T cells and serum IP-10. Thus, high iodine consumption aggravated the inflammatory reaction in the thyroid and mild high iodine consumption increased serum IP-10 levels after induction with bTg.

The accumulation of [35S]methimazole by human and rat lymphocytes

1983 ◽  
Vol 102 (1) ◽  
pp. 68-70 ◽  
Author(s):  
G. S. Shewring ◽  
J. H. Lazarus
Keyword(s):  
Antibody Production ◽  
Autoimmune Thyroiditis ◽  
Peripheral Blood ◽  
Peripheral Blood Lymphocytes ◽  
Graves Disease ◽  
Experimental Autoimmune Thyroiditis ◽  
Rat Lymphocytes ◽  
Immunosuppressive Action ◽  
Experimental Autoimmune

Abstract. The accumulation of 35S labelled methimazole (MMI) was examined in lymphocytes. No uptake of label was found in peripheral blood lymphocytes (PBL) from normal control subjects after in vitro incubation with the drug. Following administration of [35S]MMI to patients with Graves' hyperthyroidism PBL cell to plasma (C/P) 35S activity was greater than 1 in 4 of 11 patients and only in 1 of 7 other patients undergoing thyroidectomy. Thyroid lymphocytes from 2 of these patients showed some accumulation of activity. Following administration of [35S]MMI to normal rats C/P 35S ratios ranged from 1–5.6 but no 35S accumulation was found in PBL or thyroid lymphocytes from August strain rats in which experimental autoimmune thyroiditis had been produced. It is concluded that there is minimal, if any, significant accumulation of MMI in lymphocytes of patients with Graves' disease. The immunosuppressive action of MMI on lymphocyte antibody production must therefore by indirect.

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