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  • Aanaes, K, et al. (författare)
  • Extensive Endoscopic Image-Guided Sinus Surgery Decreases BPI-ANCA in Patients with Cystic Fibrosis
  • 2012
  • Ingår i: Scandinavian Journal of Immunology. - : Blackwell Publishing. - 0300-9475 .- 1365-3083. ; 76:6, s. 573-579
  • Tidskriftsartikel (refereegranskat)abstract
    • Antineutrophil cytoplasm autoantibodies (ANCA) directed against bactericidal/permeability-increasing protein (BPI) are common in patients with cystic fibrosis (CF), and serum levels are correlated with lung colonization by Pseudomonas aeruginosa and the severity of lung damage. The production of BPI-ANCA may be due to the costimulation of BPI when mounting an immune response against P. aeruginosa. The effect of surgery aiming to eradicate bacteria and infected tissue on BPI-ANCA levels is sparsely described. A cohort of patients with CF were included: 53 patients having extensive image-guided sinus surgery (EIGSS) with topical postoperative antibiotic treatment, 131 non-operated controls and 36 who had double lung transplantation (LTX). In all 219 patients, serum samples before and after surgery or at similar intervals were analysed for IgG and IgA BPI-ANCA. The EIGSS group showed a highly significant decrease in both IgA and IgG BPI-ANCA levels compared with their own preoperative values and control group values (P andlt; 0.0010.02). The LTX patients also showed a highly significant decrease in both IgA and IgG BPI-ANCA levels (P andlt; 0.001). EIGSS and LTX decrease IgA and IgG BPI-ANCA levels in patients with CF, indicating that extensive removal of infected tissue influences the pathogenic process of autoantibody production. The results shown herein are in favour of applying EIGSS in selected patients with CF and for using BPI-ANCA as a surrogate marker for guiding further therapeutic interventions.
  • Adlesic, M., et al. (författare)
  • Histamine in rheumatoid arthritis
  • 2007
  • Ingår i: Scandinavian Journal of Immunology. - : Wiley-Blackwell. - 1365-3083. ; 65:6, s. 530-7
  • Tidskriftsartikel (refereegranskat)abstract
    • Rheumatoid arthritis (RA) is an autoimmune disease characterized by a persistent inflammation of the synovium, leading to the erosion of articular cartilage and bone. Synovial mast cells and their effector molecule, histamine, receive increased attention as mediators of joint inflammation. The aim of our study was to analyse levels of free histamine in serum and joint fluid of RA patients and to evaluate the potential inflammatogenic properties of histamine in vivo and in vitro. Histamine levels were measured by an ELISA in synovial fluid and sera of RA patients and of healthy controls. Histamine levels were also assessed in plasma of RA patients undergoing anti-TNF-alpha treatment. In the murine part of the study, histamine was injected intra-articularly in the knee joint of mice and the joints were subsequently analysed with respect to induction of inflammation. RA patients displayed significantly lower levels of histamine in circulation (0.93 +/- 0.16 ng/ml) compared with the healthy controls (1.89 +/- 0.45 ng/ml, P < 0.001). Locally, in synovial fluid the levels of histamine were even lower (0.37 +/- 0.16 ng/ml, P < 0.0006). Long-term anti-TNF-alpha treatment significantly increased circulating levels of histamine in RA patients. Our experiments on animals show that histamine on its own neither induces inflammation in the joint cavity nor influences the course of HMGB1 and peptidoglycan-induced joint inflammation. Based on our experimental and clinical studies we suggest that histamine lacks harmful properties in RA.
  • Babiker-Mohamed, H, et al. (författare)
  • Characterization of monoclonal anti-alpha 1-microglobulin antibodies : binding strength, binding sites, and inhibition of lymphocyte stimulation
  • 1991
  • Ingår i: Scandinavian Journal of Immunology. - : Wiley-Blackwell. - 1365-3083. ; 34:5, s. 655-666
  • Tidskriftsartikel (refereegranskat)abstract
    • Eleven monoclonal antibodies (MoAb) directed against the immunoregulatory plasma glycoprotein alpha 1-microglobulin were characterized. The MoAb were produced in mice immunized with a mixture of alpha 1-microglobulin homologues from man, guinea pig, rat and rabbit. Using radioimmunoassay, western blotting, affinity chromatography, and Scatchard analysis, the affinities and binding sites of the MoAb were analysed. All antibodies were more or less cross-reactive, but most showed a major specificity for one or two of the alpha 1-microglobulin homologues. None of the antibodies was directed against the carbohydrate moiety of alpha 1-microglobulin. Six of the MoAb had high affinity for the antigen and four of these were directed towards the same part of the molecule though differing in their species specificity. Five showed lower affinity for the antigen and were mainly directed towards epitopes on other parts of the molecule. Only some of the antibodies could block the proliferation of lymphocytes induced by human alpha 1-microglobulin. The blocking efficiency of the different antibodies was similar when tested on the stimulation of human or mouse lymphocytes, suggesting that the same part of the alpha 1-microglobulin molecule is responsible in both species. The magnitude of blocking by the different MoAb was not related to their affinities, emphasizing the importance of where on the alpha 1-microglobulin molecule, rather than how strongly, they bind. The binding of the strongest blocking antibody was shown to be directed to a C-terminal peptide of rat alpha 1-microglobulin, indicating that this part of alpha 1-microglobulin is important for the mitogenic effects. Thus the panel of anti-alpha 1-microglobulin MoAb should be a valuable tool for structural and functional studies of alpha 1-microglobulin.
  • Badn, Wiaam, et al. (författare)
  • Inhibition of Inducible Nitric Oxide Synthase Enhances Anti-tumour Immune Responses in Rats Immunized with IFN-gamma-Secreting Glioma Cells.
  • 2007
  • Ingår i: Scandinavian Journal of Immunology. - : Wiley-Blackwell. - 1365-3083. ; 65:3, s. 289-297
  • Tidskriftsartikel (refereegranskat)abstract
    • Interferon gamma (IFN-gamma) has successfully been used in immunotherapy of different experimental tumours. Mechanistically, IFN-gamma has extensive effects on the immune system including release of nitric oxide (NO) by upregulation of the inducible nitric oxide synthase (iNOS). NO has putative immunosuppressive effects but could also play a role in killing of tumour cells. Therefore, the aim of the present study was to clarify whether inhibition of iNOS in rats immunized with glioma cells (N32) producing IFN-gamma (N32-IFN-gamma), could enhance the anti-tumour immune response. Initially, both a selective iNOS, L-N-6-(I-Iminoethyl)-L-lysine (L-NIL), and non-selective, N-nitro-L-arginine methyl ester (L-NAME), inhibitor of NOS were tested in vitro. After polyclonal stimulation with LPS and SEA, both L-NIL and L-NAME enhanced proliferation and production of IFN-gamma from activated rat splenocytes and this effect was inversely correlated to the production of NO. However, L-NIL had a broader window of efficacy and a lower minimal effective dose. When rats were immunized with N32-IFN-gamma), and administered NOS inhibitors by intraperitoneal (i.p.) mini-osmotic pumps, only splenocytes of rats treated with L-NIL, but not L-NAME, displayed an enhanced proliferation and production of IFN-gamma when re-stimulated with N32 tumour cells. Based on these findings, L-NIL was administered concurrently with N32-IFN-gamma cells to rats with intracerebral (i.c.) tumours resulting in a prolonged survival. These results show that inhibition of iNOS can enhance an IFN-gamma-based immunotherapy of experimental i.c. tumours implying that NO released after immunization has mainly immunosuppressive net effects.
  • Bennett, Matthew, et al. (författare)
  • Was it there all the time?
  • 2003
  • Ingår i: Scandinavian Journal of Immunology. - : Wiley-Blackwell. - 1365-3083. ; 57:6, s. 499-505
  • Forskningsöversikt (refereegranskat)abstract
    • The complement system is old, yet it may still have something new to teach us. For many years, research has existed which shows that C3d, in addition to its established role as an adjuvant, could have an immunosuppressive activity. Being true, it suggests that a common mechanism may be used both by organisms and by their pathogens to prevent unwanted immune responses.
  • Björck, Lars, et al. (författare)
  • On the interaction between beta 2-microglobulin and group A streptococci
  • 1984
  • Ingår i: Scandinavian Journal of Immunology. - : Wiley-Blackwell. - 1365-3083. ; 20:1, s. 69-79
  • Tidskriftsartikel (refereegranskat)abstract
    • beta 2-microglobulin (beta 2m) was found to interact with many group A streptococcal strains. The interaction appeared to require multipoint attachment, since monomeric beta 2m in solution showed no binding, whereas both beta 2m monomers bound to liposomes, and beta 2m in aggregates showed affinity for the bacteria. Aggregated HLA antigens (-A, -B and -C) and aggregated beta 2m exhibited the same binding patterns when tested in binding experiments with various group A streptococcal strains. Furthermore, beta 2m aggregates in excess completely blocked the binding of aggregated HLA antigens, thereby demonstrating that beta 2m is able to interact with streptococcal surface structures also when it is part of the HLA antigen complex. M protein-positive group A streptococcal strains bound significantly more beta 2m than M protein-negative variants of these strains. Purified M 12 protein partly inhibited the binding of radiolabelled beta 2m aggregates to whole streptococci, and in gel filtration and affinity chromatography experiments, the M 12 protein interacted with beta 2m. These various data suggest that the interaction between beta 2m and group A streptococci could be mediated by M protein. Lipoteichoic acid (LTA) is a constituent of the streptococcal cell wall that has been reported to form complexes with M protein at the bacterial cell surface. However, LTA did not influence the interaction between beta 2m and streptococci, suggesting that the binding of beta 2m to streptococcal M protein represents a pure protein-protein interaction. In vivo such an interaction could be established between infecting streptococci and host cells. Among 45 strains of different M types large differences in beta 2m binding were recorded, whereas among 60 strains of the classical nephritogenic M types 12 and 49, all were highly beta 2m-reactive, which points towards a role for beta 2m in streptococcal pathogenicity.
  • Carlsén, Maria, et al. (författare)
  • Evidence for De Novo Expression of Thymic Insulin by Peripheral Bone Marrow-derived Cells.
  • 2008
  • Ingår i: Scandinavian Journal of Immunology. - : Wiley-Blackwell. - 1365-3083. ; 68, s. 67-74
  • Tidskriftsartikel (refereegranskat)abstract
    • Thymic expression of insulin has been suggested to play a major role in negative selection of autoreactive T cells and tolerance induction against pancreatic beta cells. Furthermore, the expression of insulin in peripheral antigen-presenting cells (APC) has been clearly demonstrated but whether thymic negative selection and tolerance induction also depends on peripheral influx of self-antigens (Ag) remains to be conclusively demonstrated. In this study, we wanted to test whether peripheral influx of insulin expressing cells might contribute to negative selection. In order to address this question, we used mice deficient in the Ins1 and Ins2 genes. Embryonic thymi either deficient in both insulin genes or expressing Ins2 were dissected and transplanted under the kidney capsule of athymic nude mice recipients. After indicated time points, grafted thymi were removed and analysed for insulin re-expression and for the emergence of autoreactive T cells. The analysis revealed a re-expression of Ins2 in grafted insulin deficient thymi suggesting that self-Ag expression in the thymus is not only intrinsically regulated but peripheral influx of APC capable of expressing insulin might contribute to thymic selection and tolerance induction.
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