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  • 1
    Language: English
    In: European Journal of Immunology, April 2002, Vol.32(4), pp.1021-1028
    Description: Experimental autoimmune thyroiditis (EAT) is inducible in mice by immunization with thyroglobulin and adjuvant. Previous studies have shown that EAT is an autoimmune Th1‐mediated disease but its characteristics differ with the adjuvant. Granulomatous lesions with marked follicular disruption develop following administration of thyroglobulin (Tg) and complete Freund's adjuvant (CFA) whereas when lipopolysaccharide (LPS) is used as the adjuvant only focal infiltrates of mononuclear cells are observed. The pro‐inflammatory cytokine, TNF‐α, is associated with Th1 autoimmune‐mediated conditions. Cytokine antagonists have been used as potential therapeutic agents in several experimental autoimmune models. Soluble cytokine receptors belong to this category and may naturallybe shed from cell membranes to inhibit cytokine activity. We show that the administration of the soluble TNF receptor type I (sTNFR I) in the induction of EAT has very different effects on the two models of induced autoimmune thyroiditis. sTNFR I treatment inhibits the induction of EAT only when mouse Tg is given with LPS not with CFA, suggesting an important difference in the pathogenic processes.
    Keywords: Soluble Tnf Receptor Type I ; Experimental Autoimmune Thyroiditis
    ISSN: 0014-2980
    E-ISSN: 1521-4141
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  • 2
    Language: English
    In: European Journal of Immunology, August 2003, Vol.33(8), pp.2278-2286
    Description: IL‐18 is a cytokine structurally and functionally related to IL‐1 that, in synergy with IL‐12, stimulates the synthesis of IFN‐γ from T lymphocytes and natural killer cells. Because IFN‐γ plays a key pathogenic role in the development of murine immunoinflammatory diabetes induced by multiple low doses of streptozotocin (STZ) we investigated the effect of negating the actions of endogenous IL‐18 in this model by administering recombinant IL‐18‐binding protein:Fc (IL‐18 bp:Fc). C57BL/6 mice were injected once daily with 40 mg/kg STZ for 5 consecutive days, day 0 being the first day of STZ challenge. Relative to control animals treated in parallel with either PBS or human IgG, mice treated from day –3 to day 7 with daily doses of 150 μg of IL‐18 bp:Fc exhibited lowerincidence of diabetes and milder insulitis. In contrast, mice that were treated with IL‐18 bp:Fc from day 7 to day 14 exhibited clinical and histological signs of STZ‐induced diabetes similar to those of control mice treated with IgG. The protective effect of IL‐18 bp:Fc was accompanied by modified immune responses, in that spleen cells and peritoneal macrophages contained fewer IFN‐γ secreting cells and released lower amounts of nitrite (an index of nitric oxide production) and IL‐1β. We conclude that intact IL‐18 function is essential for the full diabetogenic effectof low dose STZ in C57BL/6 mice.
    Keywords: Cytokines ; Immunotherapy ; Il‐18 ; Type 1 Diabetes ; Streptozotocin
    ISSN: 0014-2980
    E-ISSN: 1521-4141
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  • 3
    Language: English
    In: European Journal of Immunology, 06/1999, Vol.29(6), pp.1933-1942
    Description: Experimental autoimmune thyroid disease (EAT) can be induced experimentally in mice following immunization with mouse thyroglobulin (mTg) and the adjuvants lipopolysaccharide (LPS) or complete Freund's adjuvant (CFA). EAT can also be transferred to naive recipients by CD4 super(+) T cells from mTg-primed mice. Here we demonstrate a role for IL-12 in the development of EAT by the ability of neutralizing antibody to IL-12 to reduce disease severity and by the lack of significant levels of thyroid infiltration in IL-12p40-deficient mice following immunization with mTg and CFA. A single injection of 300 ng IL-12 at the time of initial immunization with mTg and LPS was able to increase the degree of thyroid infiltration. These data are all consistent with EAT being a Th1-mediated disease. Conversely, however, administration of IL-12 over a prolonged period markedly inhibited the induction of EAT by mTg and CFA and, if given to recipients, inhibited the transfer of EAT by mTg-primed lymph node cells. The development of an autoantibody response to mTg was also inhibited when IL-12 was administered throughout the experimental period, suggesting that sustained exposure to IL-12 can be immunosuppressive.
    Keywords: Autoimmune Diseases ; Adjuvants ; Interleukin 12 ; Autoimmune Diseases ; Adjuvants ; Interleukin 12 ; Autoimmune Diseases ; Adjuvants ; Interleukin 12 ; Others ; Interleukins ; Endocrine ; Immunology ; Lipopolysaccharides ; Mice ; Thyroid Diseases ; Immunology ; Lipopolysaccharides ; Mice ; Thyroid Diseases ; Immunology ; Lipopolysaccharides ; Mice ; Thyroid Diseases ; Immunology ; Lipopolysaccharides ; Mice ; Thyroid Diseases;
    ISSN: 0014-2980
    E-ISSN: 1521-4141
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  • 4
    Language: English
    In: European Journal of Immunology, June 1999, Vol.29(6), pp.1933-1942
    Description: Experimental autoimmune thyroid disease (EAT) can be induced experimentally in mice following immunization with mouse thyroglobulin (mTg) and the adjuvants lipopolysaccharide (LPS) or complete Freund's adjuvant (CFA). EAT can also be transferred to naive recipients by CD4 T cells from mTg‐primed mice. Here we demonstrate a role for IL‐12 in the development of EAT by the ability of neutralizing antibody to IL‐12 to reduce disease severity and by the lack of significant levels of thyroid infiltration in IL‐12p40‐deficient mice following immunization with mTg and CFA. A single injection of 300 ng IL‐12 at the time of initial immunization with mTg and LPS was able to increase the degree of thyroid infiltration. These data are all consistent with EAT being a Th1‐mediated disease. Conversely, however, administration of IL‐12 over a prolonged period markedly inhibited the induction of EAT by mTg and CFA and, if given to recipients, inhibited the transfer of EAT by mTg‐primed lymphnode cells. The development of an autoantibody response to mTg was also inhibited when IL‐12 was administered throughout the experimental period, suggesting that sustained exposure to IL‐12 can be immunosuppressive.
    Keywords: Il‐12 ; Experimental Autoimmune Thyroid Disease ; Knockout ; Isotype Switching
    ISSN: 0014-2980
    E-ISSN: 1521-4141
    Source: John Wiley & Sons, Inc.
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  • 5
    Language: English
    In: European Journal of Immunology, April 1999, Vol.29(4), pp.1342-1352
    Description: Recent studies have shown that denatured exogenous antigens can prime cytotoxic T lymphocytes (CTL). To assess the contribution of CTL to experimental autoimmune thyroiditis (EAT), porcine thyroglobulin (pTg) was heat‐denatured (hdpTg) and injected i.  v. into CBA/J mice, without the aid of adjuvants. Both lymphocytic infiltrations of the thyroid glands and levels of Tg‐specific CTL were similar to those found in conventional EAT induced by Tg and adjuvants. In contrast, proliferative responses could not be detected, and titers of antibodies to pTg were 20 times lower. These EAT‐inducer CTL belong to the CD8 cell subset and exerted their thyroiditogenic potential through release of IFN‐γ. We conclude that hdpTg‐induced EAT is mediated by type 1 cytotoxic T cells (Tc1).
    Keywords: Autoimmunity ; Tc1 ; Cytotoxic T Lymphocyte ; Animal Model
    ISSN: 0014-2980
    E-ISSN: 1521-4141
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  • 6
    Language: English
    In: European Journal of Immunology, June 1997, Vol.27(6), pp.1580-1583
    Description: Interleukin(IL)‐13, a cytokine produced by T helper 2 (Th2) cells, is a powerful inhibitor of macrophage functions, including surface expression of CD14 and production of IL‐1 and tumor necrosis factor (TNF)‐α. We tested the effects of recombinant mouse(m)IL‐13 in a neonatal mouse model of endotoxin shock; this is a macrophage‐dependent condition, which is a model of neonatal sepsis in humans. mIL‐13 (0.5 μg/mouse) dramatically reduced the lethal effects of lipopolysaccharide (LPS) if administered either 24 or 4 h prior to or concomitantly with LPS challenge. This action might be mediated by multiple modulatory activities of IL‐13 on LPS‐induced cytokine secretion since, relative to control animals, the mice treated with mIL‐13 had eight times lower peak blood levels of TNF. The IL‐1β levels were also decreased, whereas increased levels of IL‐6 and IL‐10 were observed at several time points after LPS challenge.
    Keywords: Cytokine ; Interleukin‐13 ; Sepsis ; Tumor Necrosis Factor
    ISSN: 0014-2980
    E-ISSN: 1521-4141
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  • 7
    Language: English
    In: European Journal of Immunology, May 1995, Vol.25(5), pp.1184-1190
    Description: Interferon‐γ (IFN‐γ) exerts both enhancing and suppressing influences on collagen‐induced arthritis (CIA), depending on the route and protocol of administration. To study the role of IFN‐γ on the autoimmune process of CIA, we treated DBA/1 mice with two different rat monoclonal antibodies (mAb) to murine IFN‐γ. Treatments, given twice weekly for 4 weeks, consisted of intraperitoneal injections of either mAb. In early treatments, starting from the day of immunization with type II collagen (CII), the severity of arthritis was reduced in both groups of anti‐IFN‐γ‐treated mice compared with control groups. Moreover, anti‐CII antibody levels decreased in the sera of these mice. CIA was also down‐regulated in mice treated from days 14 or 28 post immunization. In contrast, late treatments with anti‐IFN‐γ mAb either induced aggravating effects, or did not affect the course of the disease. On the other hand, administration of high doses (8 × 10 U three times/week) of rat recombinant IFN‐γ exerted a transient increase of CIA severity. These findings suggest that IFN‐γ may play a critical role during both the induction and the course of CIA, first enhancing the immune response, and then regulating the arthritis process.
    Keywords: Interferon‐Γ ; Collagen‐Induced Arthritis ; Immunotherapy
    ISSN: 0014-2980
    E-ISSN: 1521-4141
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  • 8
    Language: English
    In: European Journal of Immunology, May 2005, Vol.35(5), pp.1501-1509
    Description: Treatment (from 5 to 25 weeks of age) with a novel blocking monoclonal antibody, mAb I‐10, directed against the plasma membrane (pm) form of LAMP‐1, protected against development of autoimmune diabetes in the NOD mouse. A shorter course of treatment, from 5 to 12 weeks of age, significantly reduced the occurrence of insulitis as well as disease onset. Interfering with pm‐LAMP‐1 required continuous treatment as tolerance was not observed when treatment was stopped, and no higher proportion of cells with a T regulatory phenotype ( CD4CD25) were induced. The mechanism appears to involve modulating a proinflammatory cytokine, as the proportion of pancreatic‐infiltrating IFN‐γ‐positive cells was significantly reduced in the mAb I‐10‐treated group. These results demonstrate an unexpected role for pm‐LAMP‐1 in autoimmune disease progression, and suggest that further investigation should be performed to understand how this molecule modulates IFN‐γ‐driven responses.
    Keywords: Lamp‐1 ; Ifn‐Γ ; Th1 Cells ; Non‐Obese Diabetic Mice ; Type 1 Diabetes
    ISSN: 0014-2980
    E-ISSN: 1521-4141
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  • 9
    Language: English
    In: European Journal of Immunology, January 1993, Vol.23(1), pp.275-278
    Description: CBA/J mice immunized with thyreoglobulin (Tg) develop an experimental autoimmune thyroiditis (EAT) with lymphocytic infiltration of the thyroid glands, autoantibodies to Tg and occurrence of EAT‐specific T cells. When these mice were treated for 4 weeks after immunization with 1 mg/week of a monoclonal antibody (mAb) that neutralizes the activity of interferon‐γ (IFN) a beneficial effect on the onset of EAT was observed. Characteristic features of EAT were significantly reduced, including the lymphocytic infiltrations of the thyroid glands and the serum levels of autoantibodies to Tg. Moreover, in lymphoid organs, mAb to IFN‐γ significantly reduced the percentages of Tg‐specific CD8 cells, labeled by the anti‐clonotypic mAb AG7. These Tg‐specific T cells seem responsible for thyroid damages and disease development, since EAT was simultaneously abrogated. These results show that IFN‐γ plays an essential role in the pathophysiology of EAT and suggest the possibility to treat autoimmune thyroid diseases with mAb to IFN‐γ or drugs able to antagonize the production and/or the action of this cytokine.
    Keywords: Autoimmune Thyroidites ; Interferon‐Γ ; T Cells
    ISSN: 0014-2980
    E-ISSN: 1521-4141
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  • 10
    Language: English
    In: European Journal of Immunology, February 2000, Vol.30(2), pp.438-447
    Description: Systemic lupus erythematosus (SLE)‐prone female MRL‐lpr / lpr (MRL‐lpr) mice were treated with mouse or rat IFN‐γ under different experimental conditions, both prophylactically in 6‐ to 8 week‐old animals and therapeutically in 12‐ to 18‐week‐old SLE‐affected mice. It was found that IFN‐γ heterogeneously modulated the course of the disease in MRL‐lpr mice. When administered prophylactically, IFN‐γ favorably modulated the histological, serological and clinical signs of the disease. Relative to untreated or PBS‐treated control animals, the MRL‐lpr mice which received IFN γ were virtually free of inflammatory infiltration of the kidneys and the lungs, had lower levels of azotemia with reduction of both circulating IgG1, IgG2a and IgG3 and anti‐double strand (ds) and single strand (ss) DNA antibodies, milder skin vasculitis, significantly reduced enlargment of their lymph nodes and lower weight of the spleens. IFN‐γ also lowered the rate of mortality of MRL‐lpr mice. In contrast to these findings, therapeutically administered IFN‐γ worsened the course of the disease in MRL‐lpr mice, which exhibited increased proteinuria, higher levels of IgG2a and IgG3 and anti‐ds and ‐ss DNA antibodies, more aggressive nephritis and died at an earlier age than PBS‐treated control mice. The dichotomic effect of IFN‐γ on disease manifestation in MRL‐lpr mice offers new insights into the complex role of this cytokine in the regulation of systemic autoimmunity such as SLE.
    Keywords: Autoimmune Diseases ; Cytokine ; Ifn‐Γ ; Mrl‐Lpr Mouse ; Systemic Lupus Erythematosus
    ISSN: 0014-2980
    E-ISSN: 1521-4141
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