{"title":"In Vivo Localization of Fas-Associated Death Domain Protein in the Nucleus and Cytoplasm of Normal Thyroid and Liver Cells","authors":"L. Tourneur, A. Schmitt, G. Chiocchia","doi":"10.2174/1876894600901010027","DOIUrl":"https://doi.org/10.2174/1876894600901010027","url":null,"abstract":"FADD (Fas-associated death domain) is the main death receptor adaptor molecule that transmits apoptotic sig- nal. Recently, FADD protein was shown to be expressed both in the cytoplasm and nucleus of in vitro cell lines. In con- trast to the cytoplasmic FADD, the nuclear FADD was shown to protect cells from apoptosis. However, in vivo subcellu- lar localization of FADD was still unknown. Here, we demonstrated that FADD protein was expressed in both cytoplas- mic and nuclear compartment in ex vivo thyroid cells demonstrating that nuclear sublocalization of FADD protein was a relevant phenomenon occurring in vivo. Moreover, we showed that in the nucleus of untransformed thyroid cells FADD localized mainly on euchromatin. We confirmed the nuclear localization of FADD in ex vivo liver and showed that in this organ FADD and MBD4 interact together. These results demonstrate that FADD is physiologically expressed in the nu- cleus of cells in at least two mouse organs. This particular localization opens new possible role of FADD in vivo either as an inhibitor of cell death, or as a transcription factor, or as a molecular link between apoptosis and genome surveillance.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"1 1","pages":"27-32"},"PeriodicalIF":0.0,"publicationDate":"2009-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68150694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Al-Shukaili, J. Al-Kaabi, Saif Al-Gafri, B. Hassan, Abdullah Al-Muneeri
{"title":"Quantification of CD4+ CD25+ Regulatory T Cells in Peripheral Blood of Patients with Systemic Lupus Erythematosus and Rheumatoid Arthritis","authors":"A. Al-Shukaili, J. Al-Kaabi, Saif Al-Gafri, B. Hassan, Abdullah Al-Muneeri","doi":"10.2174/1876894600901010005","DOIUrl":"https://doi.org/10.2174/1876894600901010005","url":null,"abstract":"Recent animal studies have shown that regulatory T cells play a crucial role in the suppression of the immune response and that depletion of this subset of T cells might lead to development of autoimmune diseases. The aim of this work was to quantify regulatory T cells (CD4+ CD25+) in the peripheral blood of Omani patients with Systemic Lupus Erythematosus (SLE) and Rheumatoid arthritis (RA) and correlate these findings with the disease activity of the patients. Thirty patients with SLE, 30 patients with RA and 25 healthy volunteers were enrolled in this study. Patients were divided into highly active or low active groups, depending on the disease activity. Flow cytometer was used to quantify CD4+ CD25+ T cells in the peripheral blood mononuclear cells (PBMC). We found that both highly active SLE (0.242 ± 0.3) and RA (0.56 ± 0.29) patients had significantly (p<0.001) lower levels of CD4+CD25 bright T cells than did normal controls (1.74 ± 0.47%) or patients with low disease activity (SLE=1.54 ± 0.33, RA=1.829 ± 0.76). The decreased number of CD4+CD25 bright T cells during disease activity was restored in remitting phase of SLE patients. This data provides further evidence supporting the hypothesis of defect of regulatory T cells in SLE and RA patients; which may have an important implication in the context of the control of the inflammation and development of autoimmunity.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"1 1","pages":"5-9"},"PeriodicalIF":0.0,"publicationDate":"2009-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68150618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Bowszyc-Dmochowska, A. Seraszek, E. Kaczmarek, J. Gornowicz, M. Dmochowski
{"title":"Low Strength of Correlation between the Intensity of Neutrophil Elastase Expression in Lesional Skin and the Level of Serum IgA Antibodies to Epidermal Transglutaminase in Dermatitis Herpetiformis","authors":"M. Bowszyc-Dmochowska, A. Seraszek, E. Kaczmarek, J. Gornowicz, M. Dmochowski","doi":"10.2174/1876894600901010001","DOIUrl":"https://doi.org/10.2174/1876894600901010001","url":null,"abstract":"Whereas it has been shown that neutrophil elastase (NE) is a crucial enzyme degrading the dermal-epidermal junction (DEJ) in bullous pemphigoid (BP), experimental studies on the role of NE in dermatitis herpetiformis (DH), a disease in which, as in BP, an intra-lamina lucida blister is formed, are scanty. The aim of this study was to analyse whether there is a correlation between levels of serum IgA antibodies to the epidermal transglutaminase (TG3), an enzyme believed to be the autoantigen of DH, and expression of NE in lesional skin in DH. A series of 21 consecutive patients with DH was studied. The levels of IgA antibodies to TG3 in sera were calculated with ELISA. The expressions of NE were examined with immunohistochemical technique in sections of lesional skin using a mouse monoclonal antibody to human NE. The digital microscopic image analysis with the appropriate software was then used to measure intensities of NE expression. The correlation between the intensity of NE expression in lesional skin and the level of serum IgA anti- bodies to TG3 in DH was of low strength. Thus, it is speculated that in DH the engagement of IgA autoantibodies to the enzyme, TG3, on cutaneous neutrophils might not be a principal stimulus to releasing NE, the enzyme known to degrade DEJ in subepidermal blistering diseases with autoimmunity to DEJ structural proteins.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"1 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2009-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68150605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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