scholarly journals Death Ligand Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Inhibits Experimental Autoimmune Thyroiditis

Endocrinology ◽  
2005 ◽  
Vol 146 (11) ◽  
pp. 4721-4726 ◽  
Author(s):  
Su He Wang ◽  
Zhengyi Cao ◽  
Julie M. Wolf ◽  
Mary Van Antwerp ◽  
James R. Baker
Keyword(s):  
Autoimmune Thyroiditis ◽  
T Helper ◽  
Mononuclear Cell Infiltration ◽  
T Helper 1 ◽  
Experimental Autoimmune Thyroiditis ◽  
Cell Responses ◽  
Control Protein ◽  
Necrosis Factor ◽  
Experimental Autoimmune

The role of TNF-related apoptosis-inducing ligand (TRAIL) in autoimmune thyroiditis is unclear. We used experimental autoimmune thyroiditis to clarify the contribution of TRAIL to the development of autoimmune thyroiditis. CBA/J mice were immunized with murine thyroglobulin, and spleen cells from these mice were subsequently injected into irradiated recipient CBA/J mice. One week later, the recipient mice were treated with recombinant TRAIL or a control protein. Compared with control animals, TRAIL-treated mice developed a milder form of the disease with a significant decrease in mononuclear cell infiltration in the thyroid and less thyroid follicular destruction. Furthermore, the number of apoptotic thyrocytes and also thyroglobulin-specific T helper-1 cell responses in TRAIL-treated mice was lower than that in the control animals. This study suggests that exogenous TRAIL suppresses the development of autoimmune thyroiditis via altering the function of cells involved in the immune response. These findings may contribute toward a novel treatment autoimmune thyroiditis.

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.

Unique role of thyroxine in T cell recognition of a pathogenic peptide in experimental autoimmune thyroiditis

1996 ◽  
Vol 26 (4) ◽  
pp. 768-772 ◽  
Author(s):  
Kim I. Dawe ◽  
Patricia R. Hutchings ◽  
Mario Geysen ◽  
Brian R. Champion ◽  
Anne Cooke ◽  
...  
Keyword(s):  
T Cell ◽  
Autoimmune Thyroiditis ◽  
Cell Recognition ◽  
Experimental Autoimmune Thyroiditis ◽  
Unique Role ◽  
T Cell Recognition ◽  
Experimental Autoimmune

IL-17A, IL-22, and IL-23 as Markers of Psoriasis Activity

2015 ◽  
Vol 19 (6) ◽  
pp. 555-560 ◽  
Author(s):  
Christina Fotiadou ◽  
Elizabeth Lazaridou ◽  
Eleni Sotiriou ◽  
Spiridon Gerou ◽  
Athanasios Kyrgidis ◽  
...  
Keyword(s):  
Th17 Cells ◽  
Tumor Necrosis ◽  
Serum Levels ◽  
Sensitivity Analyses ◽  
T Helper ◽  
T Helper 1 ◽  
Factor Α ◽  
Necrosis Factor ◽  
Active Disease

Introduction: T-helper 1 (Th1), Th17 cells, and their related cytokines are implicated in psoriasis pathogenesis although the contribution of each group of cytokines in psoriasis activity has not been fully clarified. Objectives: To investigate whether Th17-related cytokines are associated with psoriasis activity. Methods: The serum levels of interleukin (IL)-1β, 6, 8, 17Α, 22, 23, and tumor necrosis factor-α (TNFα) were measured with flow cytometry in 35 patients with plaque psoriasis (21 with stable and 14 with active disease) and in 20 healthy controls. Results: Interleukin-6, 8, 17A, 22, 23, and TNFα were significantly elevated in psoriasis patients compared with controls. In the sensitivity analyses, patients with active disease showed significantly increased levels of IL-17A, IL-23, and IL-22 as compared to the group of patients with stable psoriasis. Conclusions: Our study highlights a possible crucial role of IL-17A, IL-22, and IL-23 in the activity of psoriasis and the early stages of the disease.

scholarly journals Regenerative Potentials of the Murine Thyroid in Experimental Autoimmune Thyroiditis: Role of CD24

Endocrinology ◽  
2008 ◽  
Vol 150 (1) ◽  
pp. 492-499 ◽  
Author(s):  
Cindy Y. Chen ◽  
Hiroaki Kimura ◽  
Melissa A. Landek-Salgado ◽  
Judith Hagedorn ◽  
Miho Kimura ◽  
...  
Keyword(s):  
Stem Cells ◽  
Autoimmune Thyroiditis ◽  
Hashimoto Thyroiditis ◽  
Experimental Autoimmune Thyroiditis ◽  
Normal Morphology ◽  
And Function ◽  
Infiltrating Lymphocytes ◽  
Experimental Autoimmune

Hashimoto thyroiditis can be partially reproduced in mice by immunization with thyroglobulin or, more recently, thyroperoxidase. This experimental autoimmune thyroiditis (EAT) model has been extensively characterized during early disease phases (up to d 35 after immunization). By extending the analysis of EAT to 100 d after immunization, we noted a remarkable regenerative capacity of the thyroid and the expression of Oct-4, suggesting in vivo the existence of adult thyroid stem cells. After an almost complete destruction of the follicular architecture, occurring between d 21 and 28, the thyroid was capable of restoring its follicles and reducing the mononuclear infiltration, so that by d 100 after immunization, it regained its normal morphology and function. During this regeneration process, thyrocytes expressed high levels of CD24. We therefore assessed the role of CD24 in thyroid regeneration by inducing EAT in mice lacking CD24. Regeneration was faster in the absence of CD24, likely a consequence of the effect of CD24 on the infiltrating lymphocytes. The study suggests that the EAT model can also be used as a tool to investigate adult thyroid stem cells. The murine thyroid is capable of restoring its architecture after an insult that almost completely destroys it.

scholarly journals THE ROLE OF MYCOBACTERIA AND THE EFFECT OF PROTEOLYTIC DEGRADATION OF THYROGLOBULIN ON THE PRODUCTION OF AUTOIMMUNE THYROIDITIS

1969 ◽  
Vol 130 (2) ◽  
pp. 243-262 ◽  
Author(s):  
W. O. Weigle ◽  
Gloria J. High ◽  
R. M. Nakamura
Keyword(s):  
Autoimmune Thyroiditis ◽  
Proteolytic Enzymes ◽  
Ion Concentration ◽  
Experimental Autoimmune Thyroiditis ◽  
Hydrogen Ion Concentration ◽  
Initial Event ◽  
Local Areas ◽  
Experimental Autoimmune

Data are presented which suggest that the initial event involved in experimental autoimmune thyroiditis following injection of rabbits with homologous thyroglobulin in complete Freund's adjuvant is alteration of the thyroglobulin. Alteration of the thyroglobulin does not occur during incorporation into the adjuvant or in vitro storage in the adjuvant, and the mycobacteria in the adjuvant have no direct effect on the thyroglobulin. Most likely, the alteration results from an increase in hydrogen ion concentration within cells or local areas in the granuloma and the subsequent action of proteolytic enzymes. These conditions are probably established in the granuloma as the result of neutrophilic response to the mycobacteria in the adjuvant. Rabbits injected with aqueous preparations of homologous thyroglobulin partially degraded in vitro with pepsin at acid pH produced antibody to native thyroglobulin and developed thyroiditis. Most of these rabbits responded to a subsequent injection of native thyroglobulin given 1 month later.

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