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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
101

Immunological mechanisms in systemic autoimmunity : autoantibodies and chemokines in systemic lupus erythematosus and during treatment with TNF inhibitors in rheumatoid arthritis

Eriksson, Catharina January 2011 (has links)
Background. Rheumatoid Arthritis (RA) is an autoimmune inflammatory disease that, without powerful treatment, may lead to irreversible joint damage. During the past decade, anti-cytokine therapy has become available, e.g., infliximab, a chimeric antibody targeting the pro-inflammatory cytokine TNF that has a central role in the inflammatory process in RA patients. Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease that may affect all organs and is characterized by a massive antibody production. Chemokines, chemokine receptors and lipoprotein receptor-related protein 1(CD91) are regulators of inflammation in autoimmune diseases and T-cell migration. Objectives. The aim of this study was to get a deeper understanding how TNF blocking treatment influences inflammatory mechanisms and autoantibody formation in RA with special reference to similarities and differences with SLE. Methods. In patients with RA treated with anti-TNF, and in SLE patients (ACR criteria) clinical evaluation was performed and blood samples analyzed. Autoantibodies were analyzed using indirect immunofluorescence, ELISA and multiplex flow cytometry in samples from anti-TNF treated RA patients (n=59) followed longitudinally for 54 weeks, in pre-diseased samples from SLE patients (n=38) and matched population-based controls (n=152). T-cell expression of chemokine receptors and CD91 was analyzed by flow cytometry, whilst serum levels of chemokines were determined using ELISA in anti-TNF treated RA-patients (n=24) followed longitudinally (30 weeks), and cross-sectionally in SLE-patients (n=23). Expression of mRNA for chemokines was analyzed in T-cells from SLE-patients (n=10) using PCR. Results. After treatment with infliximab, RA patients produced ANA, anti-dsDNA and anti-nucleosome antibodies, but not anti-ENA antibodies. Although these antibodies are considered typical for SLE only one patient developed a transient lupus-syndrome. Antibodies against cell nuclear antigens, including ENA, were detected several years before the first clinical symptom of SLE; anti-SSA was the earliest detectable antibody. In RA-patients before infliximab treatment, the T-cell expression of several chemokine receptors was elevated compared with healthy controls. In contrast, only one soluble chemokine, IP-10 was elevated. After treatment the levels of soluble MIP-1β, MCP-1 and IP-10, and the T-cell expression of CCR2 were decreased. In SLE-patients MIP-1β, MCP-1, SDF-1, IP-10 and RANTES in blood were elevated, whilst expression of CXCR5 and CCR6 on T-cells was lower than in healthy controls. T-cell expression of CXCR2 and CCR1 was elevated in active disease (measured as SLEDAI index), whereas the CXCR5 and CCR2 expression was lower in inactive SLE. In SLE patients with nephritis IP-10 was lower and T-cell expression of CXCR3 and CCR3 elevated compared with patients without nephritis. The expression of CD91 was higher on T-cells from patients not responsive to infliximab treatment compared with responders. Conclusion. These findings indicate that anti-TNF (infliximab) treatment in RA-patients has a major impact on the production of autoantibodies and chemokines. The autoantibody profile in infliximab-treated patients was similar to that predating disease onset in SLE patients with the exception of anti-ENA being detectable in SLE, but the development of lupus-syndromes was rare. The expression of CD91 on T-cells may predict responsiveness to infliximab. The expression of chemokine receptors in SLE- patients seemed to be related to disease activity. Anti-nuclear antibodies were detectable years before clinical disease onset in patients who developed SLE suggesting a gradual pathogenic process.
102

The role of autoantibodies in inflammatory myopathies /

Barbasso Helmers, Sevim, January 2007 (has links)
Diss. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 4 uppsatser.
103

Cutaneous lupus erythematosus and immunoreactivity in patients with Ro/SSA autoantibodies /

Popovic, Karin, January 2007 (has links)
Diss. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 6 uppsatser.
104

Immune mechanisms in atherosclerotic vascular disease /

Cvetkovic,́ Jasmina, January 2002 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 6 uppsatser.
105

A population-based study on early arthritis in southern Sweden : incidence, preceding infections, diagnostic markers and economic burden /

Söderlin, Maria. January 2003 (has links)
Diss. (sammanfattning) Linköping : Univ., 2003. / Härtill 4 uppsatser.
106

Environmental determinants associated with Type 1 diabetes-related autoantibodies in children /

Wahlberg, Jeanette, January 2005 (has links) (PDF)
Diss. (sammanfattning) Linköping : Linköpings universitet, 2005. / Härtill 5 uppsatser.
107

C-reactive protein (CRP) and anti-CRP autoantibodies in systemic lupus erythematosus : a study on the occurrence and clinical implications of anti-CRP antibodies and CRP-mediated complement activation /

Sjöwall, Christopher, January 2005 (has links)
Diss. (sammanfattning) Linköping : Linköpings universitet, 2006. / Härtill 5 uppsatser.
108

Autoantibodies and genetic variation in rheumatoid arthritis : aspects on susceptibility and disease course /

Kastbom, Alf, January 2007 (has links)
Diss. (sammanfattning) Linköping : Linköpings universitet, 2007. / Härtill 5 uppsatser.
109

Autoantibodies as markers of beta-cell autoimmunity in children /

Holmberg, Hanna, January 2006 (has links)
Diss. (sammanfattning) Linköping : Linköpings universitet, 2006. / Härtill 4 uppsatser.
110

Tumour biological factors characterizing metastasizing serotonin-producing ileocaecal carcinoids /

Cunningham, Janet Lynn, January 2007 (has links)
Diss. (sammanfattning) Uppsala : Uppsala universitet, 2007. / Härtill 4 uppsatser.

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