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  • 1. Asplund, A. C.
    et al.
    Falk, Elin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Molecular tools.
    Moens, Lotte
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Molecular tools.
    Kumar, Y.
    Bauser, C.
    Bernatowska, E.
    Nilsson, Mats
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Molecular tools.
    Smith, C. I. E.
    Large-scale mutation analysis of primary immunodeficiency patients by next-generation sequencing2012In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 32, no Suppl 1, p. 227-228Article in journal (Other academic)
  • 2. Gong, J
    et al.
    Larsson, R
    Ekdahl, K N
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Mollnes, T E
    Nilsson, U
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Nilsson, B
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Tubing loops as a model for cardiopulmonary bypass circuits: both the biomaterial and the blood-gas phase interfaces induce complement activation in an in vitro model.1996In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 16, no 4, p. 222-223Article in journal (Refereed)
    Abstract [en]

    We describe here a model for the study of blood/surface and blood/air interaction as encountered in cardiopulmonary bypass (CPB) circuits. Polyethylene tubing was filled with serum or blood and closed end to end into loops whereby the volume of the remaining air bubble was inversely varied with respect to that of the fluid. The loops were rotated vertically in a water bath at 37 degrees C. The profiles of C3a, iC3, and TCC generation were similar to those observed at surgery, involving CPB. Soluble heparin and heparan sulfate inhibited both C3a and TCC formation, but surface-conjugated heparin had only a minor effect. Binding of C3 and/or C3 fragments to the heparin surface was much reduced compared to the amine matrix to which heparin was linked, but compared with the polyethylene surface the effect was less pronounced. These data suggest that, in addition to the biomaterial surface, the blood-gas interface seems to play an important role in the activation of complement and that this activation is inhibitable by high concentrations of soluble glucose aminoglycans.

  • 3.
    Karlberg, Mats
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Xiang, Zou
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Nilsson, Gunnar
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Fc gamma RI-Mediated activation of human mast cells promotes survival and induction of the pro-survival gene bfl-12008In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 28, no 3, p. 250-255Article in journal (Refereed)
    Abstract [en]

    Activation of mast cells through either Fc epsilon RI or Fc gamma RI leads to release of mediators contributing to the inflammatory response. One of the biologic characteristics of mast cells in allergic pathology is that these cells have the capacity to recover and regranulate after aggregation of Fc epsilon RI. We have previously demonstrated that the prosurvival protein A1/Bfl-1 is required for mast cells to survive IgE-mediated activation. In the present study, we have investigated whether human mast cells show similar induction of bfl-1 and activation-induced survival after aggregation of Fc gamma RI. Human cord blood-derived mast cells were activated by aggregation of either Fc epsilon RI or Fc gamma RI, and activation-induced survival and induction of bfl-1 was measured. We found that aggregation of Fc gamma RI-induced expression of bf-1 and caused a comparable activation-induced mast cell survival as Fc epsilon RI does. These data suggests that activation through Fc-receptors contribute to mast cell survival during antibody-dependent mast cell mediated inflammatory responses.

  • 4.
    Lidehäll, Anna Karin
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology, Clinical Immunology.
    Sund, Fredrik
    Divisions of Infectious Diseases, University Hospital, Uppsala, Sweden.
    Lundberg, Tobias
    Divisions of Clinical Immunology and Transfusion Medicine, University Hospital, Uppsala, Sweden.
    Eriksson, Britt-Marie
    Divisions of Infectious Diseases, University Hospital, Uppsala, Sweden.
    Tötterman, Thomas H.
    Divisions of Clinical Immunology and Transfusion Medicine, University Hospital, Uppsala, Sweden.
    Korsgren, Olle
    Divisions of Clinical Immunology and Transfusion Medicine, University Hospital, Uppsala, Sweden.
    T cell control of primary and latent cytomegalovirus infections in healthy subjects2005In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 25, no 5, p. 473-481Article in journal (Refereed)
    Abstract [en]

    The T cell repertoire required to control acute and latent CMV infection in otherwise healthy individuals was examined using both functional analysis and a wide range of MHC I tetramers. Both frequency and function of CMV specific T cells varied considerably between subjects, however, within subjects values remained stable over time. In total 16 ± 3.5 CMV specific T cells/μl blood was detected, with obvious immunodominance between different CMV epitopes. Most subjects with latent infection showed low CMV specific T cell activity, whereas a subgroup (1/3) of individuals was high in either frequency or function of their CMV specific T cells. Patients with acute infection displayed high initial, but rapidly decreasing, numbers of CMV specific cells. In conclusion, a majority of healthy individuals readily seem to control latent CMV infection, whereas a subpopulation (1/3) of individuals uses a large proportion of their CD8+ T cell repertoire to control the infection.

  • 5. Lim, C.
    et al.
    Dahle, C.
    Elvin, K.
    Andersson, B.
    Rönnelid, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Truedsson, L.
    Hammarstrom, L.
    Evaluation of Reversal of IGAD: Relevance for the Diagnosis in Children2014In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 34, no S2, p. S357-S357, article id ESID-0625Article in journal (Other academic)
  • 6. Lim, Che Kang
    et al.
    Dahle, Charlotte
    Elvin, Kerstin
    Andersson, Bengt A
    Rönnelid, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Melén, Erik
    Bergström, Anna
    Truedsson, Lennart
    Hammarström, Lennart
    Reversal of Immunoglobulin A Deficiency in Children2015In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 35, no 1, p. 87-91Article in journal (Refereed)
    Abstract [en]

    PURPOSE: Immunoglobulin A deficiency (IgAD) is the most common primary immunodeficiency in the general population. It is defined as a serum IgA level below or equal to 0.07 g/l with normal IgM and IgG levels in children over the age of 4. However, a few cases of reversal of IgAD at later ages have been observed previously, especially in pediatric patients. This study aimed at investigating the frequency of reversal in a large cohort of children and young adults in order to evaluate the present definition of IgAD.

    METHODS: Clinical laboratory records from 654 pediatric IgA deficient patients, 4-13 years of age, were retrieved from five university hospitals in Sweden. Follow up in the children where IgA serum levels had been routinely measured was subsequently performed. In addition, follow up of the IgA-levels was also performed at 4, 8 and 16 years of age in children who were IgA deficient at the age of 4 years in a Swedish population-based birth cohort study in Stockholm (BAMSE).

    RESULTS: Nine out of 39 (23.1 %) children who were identified as IgAD at 4 years of age subsequently increased their serum IgA level above 0.07 g/L. The average age of reversal was 9.53 ± 2.91 years. In addition, 30 out of the 131 (22.9 %) children with serum IgAD when sampled between 5 and 9.99 years of age reversed their serum IgA level with time. The BAMSE follow up study showed a reversal of IgAD noted at 4 years of age in 8 out of 14 IgAD children at 16 years of age (5 at 8 years of age) where 4 were normalized their serum IgA levels while 4 still showed low serum levels of IgA, yet above the level defining IgAD. The results indicate that using 4 years of age, as a cut off for a diagnosis of IgAD may not be appropriate.

    CONCLUSIONS: Our findings suggest that a diagnosis of IgAD should not be made before the early teens using 0.07 g/L of IgA in serum as a cut off.

  • 7.
    Lundgren, Magnus
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Infectious Diseases.
    Darnerud, Per Ola
    Blomberg, Jonas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical Virology.
    Friman, Göran
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Infectious Diseases.
    Ilbäck, Nils-Gunnar
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Infectious Diseases.
    Sequential changes in serum cytokines reflect viral RNA kinetics in target organs of a coxsackievirus B infection in mice2009In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 29, no 5, p. 611-9Article in journal (Refereed)
    Abstract [en]

    INTRODUCTION: The pattern of cytokine responses related to viral replication during the course of the common human coxsackievirus B3 (CVB3) infection is not known. METHODS: Serum levels of 21 cytokines and chemokines were studied (Luminex technique) in CVB3-infected in mice on days 3, 6, and 9 post-infection (p.i.). CVB3 was measured quantitatively (reverse transcriptase polymerase chain reaction) in the liver and pancreas. RESULTS: Virus levels peaked on day 3 in both the liver and pancreas, but were 1,000-fold higher in the pancreas. IL-17alpha, IFN-gamma, KC, MCP-1, MIP1beta, and RANTES were detected on all days. On day 3 p.i., IL-6, IL-12(p40), KC, MCP-1, RANTES, and TNF-alpha were found to peak. On day 6 p.i., IL-1beta, IL-9, IL-12(p70), IL-13, IL-17alpha, and IFN-gamma peaked. On day 9 p.i., MIP1beta, IL-1beta, MCP-1, and TNF-alpha were still increased. These changes in cytokines may be used to monitor the progress of enteroviral infections in clinical settings.

  • 8.
    Nilsson, B
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Bjelle, A
    Lööf, L
    Nilsson, U R
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Quantitation and antigenic characterization of bound C3 of circulating immune complexes in systemic lupus erythematosus, rheumatoid arthritis, and primary biliary cirrhosis.1987In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 7, no 5, p. 420-426Article in journal (Refereed)
    Abstract [en]

    In recent years defective function of the complement-mediated clearance of immune complexes (IC) has been reported in patients with immune complex disease. The defect has been found at different levels in the clearance system. An important event in this sequential system is the binding of C3-coated particles to C3 receptors on erythrocytes and phagocytes. This study focuses on immunochemical properties of IC-bound C3 that reflect the functional state of the molecule. Sera from patients with primary biliary cirrhosis (PBC), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE) and from normal subjects were analyzed for their level of C3 precipitable in 2.7% (w/v) polyethylene glycol (PEG). The mean levels for the patient categories were significantly higher than that for the normal subjects. The immunochemical study revealed several differences among the different forms of PEG-precipitable C3. All forms expressed C3(D) antigens which are expressed by immune complex-associated and denatured forms but not by soluble physiological forms of C3. The expression of these antigens was proportionately lower for the complex-associated C3 of PBC compared to that of RA and SLE. Furthermore, employing monoclonal anti-C3(D) antibodies against the C3c and the C3d domain, distinct differences could be detected among all forms of PEG-precipitable C3. Sera from RA and SLE, in particular, contained PEG-precipitable C3 that exhibited distinctive immunochemical features with respect to these epitopes.

  • 9.
    Prokopec, Kajsa E.
    et al.
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Cell and Molecular Biology.
    Berntson, Lillemor
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Pediatrics.
    Öman, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Kleinau, Sandra
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Cell and Molecular Biology, Chemical Biology.
    Up Regulated Complement and Fc Receptors in Juvenile Idiopathic Arthritis and Correlation with Disease Phenotype2012In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 32, no 3, p. 540-550Article in journal (Refereed)
    Abstract [en]

    PURPOSE: The progress in identifying immunological mechanisms in juvenile idiopathic arthritis (JIA) has partly been hampered by the fact that the disease is heterogeneous. Here we have investigated complement and Fc receptors, as part of the inflammatory process, in two subgroups of JIA.

    METHODS: Blood from 26 patients with oligoarticular or polyarticular course type JIA and 21 healthy age and sex-matched controls were investigated by FACS and immunoassays.

    RESULTS: Increased numbers of monocytes and augmented plasma levels of C-reactive protein, C3a and IgG were found in both JIA subgroups. However, only polyarticular patients exhibited increased expression of Fc gamma receptor (FcγR) II and III and complement receptor (CR) 1 on monocytes along with enhanced CR1 expression on B cells. A correlation was observed between degree of receptor expression and C3a levels in the patients.

    CONCLUSIONS: Complement and Fc receptors are up regulated in children with multiple joint involvements, thus highlighting these pathways in the pathogenesis of polyarticular JIA.

  • 10. Sassi, A.
    et al.
    Fliegauf, M.
    Yang, L.
    Wu, G.
    Haslam, S. M.
    Mellouli, F.
    Patiroglu, T.
    Unal, E.
    Ozdemir, M. A.
    Jouhadi, Z.
    Khadir, K.
    Ben-Khemis, L.
    Ben-Ali, M.
    Ben-Mustapha, I.
    Borchani, L.
    Khemiri, M.
    Maul-Pavicic, A.
    Rakhmanov, M.
    Henneke, P.
    Kraus, H.
    Eibel, H.
    Koelsch, U.
    Nadifi, S.
    Nilsson, Mats
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Molecular tools.
    Bejaoui, M.
    Schaeffer, A. A.
    Smith, C. I. E.
    Dell, A.
    Barbouche, M. R.
    Grimbacher, B.
    Hypomorphic Homozygous Mutations in Phosphoglucomutase3 Impair Immunity and Increase Serum IGE Levels2014In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 34, p. S161-S162Article in journal (Other academic)
  • 11. Staff, Caroline
    et al.
    Magnusson, Carl G. M.
    Hojjat-Farsangi, Mohammad
    Mosolits, Szilvia
    Liljefors, Maria
    Frödin, Jan-Erik
    Wahrén, Britta
    Mellstedt, Håkan
    Ullenhag, Gustav J.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science, Oncology.
    Induction of IgM, IgA and IgE Antibodies in Colorectal Cancer Patients Vaccinated with a Recombinant CEA Protein2012In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 32, no 4, p. 855-865Article in journal (Refereed)
    Abstract [en]

    Previous clinical studies have indicated that natural IgM antibodies have the ability to induce apoptosis of tumor cells but IgE and IgA may also mediate tumor cell killing (in addition to IgG). The aim of the study was to analyse induction of IgM, IgA and IgE antibodies in patients vaccinated with the tumor associated antigen CEA. Twenty-four resected CRC patients without macroscopic disease were immunized seven times with CEA +/- GM-CSF. Four different dose schedules were used over a 12-month period. IgM, IgA and IgE antibody responses against recombinant CEA were determined by ELISA. Patients were monitored immunologically for 36 months and clinically for 147 months. GM-CSF significantly augmented the anti-CEA response for all three antibody classes. Low dose of CEA tended to induce a higher IgM, IgA or IgE anti-CEA antibody response than higher. Anti-CEA IgA antibodies could lyse CEA positive tumor cells in antibody dependent cellular cytotoxicity (ADCC) as well as in complement dependent cytotoxicity (CDC). A significant correlation between survival and high IgA anti-CEA titers was noted (p = 0.02) irrespective of GM-CSF treatment. The observation that IgA anti-CEA antibodies were cytotoxic and associated with improved survival might indicate that also these antibodies may exert a clinical anti-tumor effect.

  • 12. Strandberg, Linn
    et al.
    Ambrosi, Aurelie
    Espinosa, Alexander
    Ottosson, Lars
    Eloranta, Maija-Leena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Zhou, Wei
    Elfving, Ase
    Greenfield, Edward
    Kuchroo, Vijay K.
    Wahren-Herlenius, Marie
    Interferon-alpha induces up-regulation and nuclear translocation of the Ro52 autoantigen as detected by a panel of novel Ro52-specific monoclonal antibodies2008In: Journal of Clinical Immunology, ISSN 0271-9142, E-ISSN 1573-2592, Vol. 28, no 3, p. 220-31Article in journal (Refereed)
    Abstract [en]

    Interferon-alpha (IFN-alpha) has been implicated in the pathogenesis of Sjögren's syndrome and systemic lupus erythematosus. Ro52, which was recently identified as an E3 ligase with anti-proliferative and pro-apoptotic properties, is a major autoantigen targeted in both these conditions. Microarray analyses have indicated up-regulation of Ro52 by IFN-alpha, and the objective of the present study was to address the potential link between IFN-alpha and Ro52. To investigate the influence of IFN-alpha on Ro52 protein levels and cellular localization, we generated a panel of monoclonal antibodies to different domains of Ro52. These novel monoclonal antibodies were characterized by immunoprecipitation, Western blot, and enzyme-linked immunosorbent assay using cell lysates, recombinant Ro52 protein, and synthetic peptides. Ro52 was up-regulated in HeLa cells and human B cells at the messenger RNA and protein levels in response to IFN-alpha stimulation as detected by reverse transcriptase polymerase chain reaction and Western blot. After up-regulation, Ro52 translocated from the cytoplasm to the nucleus. The nuclear translocation of Ro52 was observed after staining with generated monoclonal antibodies specific for both the RING, coiled-coil, and B30.2 domains of Ro52 and the nuclear translocation of Ro52 preceded IFN-alpha-induced apoptotic cell death detected by caspase-3 and TUNEL staining in the treated cultures. In conclusion, our data show that IFN-alpha first induces up-regulation of Ro52 protein and then prompts translocation of the up-regulated Ro52 protein in to the nucleus. The translocation precedes apoptosis of the IFN-alpha exposed cells, suggesting a role for Ro52 in mediating the anti-proliferative or pro-apoptotic effects of the autoimmune-related cytokine IFN-alpha.

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