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  • 101.
    Stejskal, Vera
    et al.
    Stockholm University, Faculty of Science, The Wenner-Gren Institute, Immunology.
    Öckert, Karin
    Björklund, Geir
    Metal-induced inflammation triggers fibromyalgia in metal-allergic patients2013In: Neuro - endocrinology letters, ISSN 0172-780X, Vol. 34, no 6, p. 559-565Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Fibromyalgia (FM) is a disease of unknown etiology. Inflammation could be one of the mechanisms behind this disease. OBJECTIVES: We studied the frequency and clinical relevance of metal allergy in FM patients. METHODS: Fifteen female FM patients were included in the study. Metal allergy was measured by a lymphocyte transformation test, MELISA (R). Ten healthy age-matched women were used as controls for in vitro studies. Reduction of metal exposure in the FM patients was achieved by replacement of dental metal restorations and by the avoidance of known sources of metal exposure. Objective health assessment was performed 5 years after treatment. Subjective health assessment was established by a questionnaire, completed 2, 5 and in some cases 10 years after the start of the study. Follow-up MELISA was also performed. RESULTS: All FM patients tested positive to at least one of the metals tested. The most frequent reactions were to nickel, followed by inorganic mercury, cadmium and lead. Some healthy controls responded to inorganic mercury in vitro but most of the tests were negative. Objective examination 5 years later showed that half of the patients no longer fulfilled the FM diagnosis, 20% had improved and the remaining 30% still had FM. All patients reported subjective health improvement. This correlated with the normalisation of metal-specific responses in vitro. CONCLUSION: Metal allergy is frequent in FM patients. The reduction of metal exposure resulted in improved health in the majority of metal-sensitized patients. This suggests that metal-induced inflammation might be an important risk factor in a subset of patients with FM.

  • 102.
    Sverremark-Ekström, Eva
    Stockholm University, Faculty of Science, The Wenner-Gren Institute , Immunology.
    CD30 expression in relation to atopic heredity and allergic disease during childhood.2009In: Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology, ISSN 1399-3038, Vol. 20, no 2, p. 204-5Article in journal (Refereed)
  • 103.
    Sverremark-Ekström, Eva
    Stockholm University, Faculty of Science, The Wenner-Gren Institute , Immunology.
    Division of cytokines into TH1/TH2: a word of caution.2010In: Reproductive sciences (Thousand Oaks, Calif.), ISSN 1933-7205, Vol. 17, no 4, p. 318-9Article in journal (Refereed)
  • 104.
    Söderlund, Ankie
    Stockholm University, Faculty of Science, The Wenner-Gren Institute, Immunology.
    Cytokine studies in the generation and treatment of IgE-mediated allergy2002Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    So called Th2 cytokines, such as IL-4 and IL-13 are responsible for the formation of IgE antibodies, the effector antibody in atopic allergy. Cytokines of Th1 type, for example IFN-g, inhibit these responses. This thesis describes work aimed at elucidating the cytokine production underlying IgE-mediated allergy.

    Allergen specific immunotherapy (SIT) is an effective form of treatment for IgE-mediated allergy. The cytokine production in peripheral blood mononuclear cells (PBMC) taken from atopic individuals undergoing allergen SIT or placebo treatment was investigated. An increased number of IL-4- and IL-13-producing PBMC was observed during the pollen season in placebo-treated individuals, whereas in patients receiving allergen SIT, this increase was absent. Thus, in line with other studies, our findings suggest that allergen SIT exerts its effect on allergen specific T cells.

    Most IgE-mediated allergies develop during early childhood. Therefore, it is of major importance to understand the regulation of these initial immune responses. Cord blood mononuclear cells (CBMC) were collected from newborns and divided into three different groups, those with double atopic, maternal atopic or no atopic heredity. Following PHA stimulation in vitro, the ratio of IL-4-/IFN-g-producing CBMC was significantly higher in the group with double atopic heredity than in the group without. This suggests a strong genetic influence on cytokine-producing cells in the newborn. Large numbers of IL-12-producing CBMC were induced following allergen stimulation. This finding is in contrast to the general idea about deficient Th1- and Th1-inducing responses in cord blood.

    The soluble form of CD14, an endotoxin receptor involved in innate immune responses, have been negatively associated with levels of total serum IgE. We investigated whether any differences in soluble or membrane bound CD14 could be detected already in cord blood, and whether these levels were related to those in the mothers or in the same child at two years of age. We could not confirm any negative association between total serum IgE levels and sCD14. With regard to atopy, higher levels of sCD14 were found in atopic mothers compared to non-atopic, and the same was true for the cord blood of their corresponding children. The membrane bound form of CD14 was higher on cord blood cells than on cells taken from mothers or two-year-olds, whereas the opposite was observed for sCD14. These findings suggest that the initial role of CD14 might be in the early maturation and differentiation events of the immune system.

  • 105. Tangteerawatana, Piyatida
    et al.
    Perlmann, Hedvig
    Stockholm University, Faculty of Science, The Wenner-Gren Institute , Immunology.
    Hayano, Masashi
    Stockholm University, Faculty of Science, The Wenner-Gren Institute , Immunology.
    Kalambaheti, Thareerat
    Troye-Blomberg, Marita
    Stockholm University, Faculty of Science, The Wenner-Gren Institute , Immunology.
    Khusmith, Srisin
    IL4 gene polymorphism and previous malaria experiences manipulate anti-Plasmodium falciparum antibody isotype profiles in complicated and uncomplicated malaria.2009In: Malaria Journal, ISSN 1475-2875, E-ISSN 1475-2875, Vol. 8, no 1, p. 286-Article in journal (Refereed)
    Abstract [en]

    ABSTRACT: BACKGROUND: The IL4-590 gene polymorphism has been shown to be associated with elevated levels of anti-Plasmodium falciparum IgG antibodies and parasite intensity in the malaria protected Fulani of West Africa. This study aimed to investigate the possible impact of IL4-590C/T polymorphism on anti-P. falciparum IgG subclasses and IgE antibodies levels and the alteration of malaria severity in complicated and uncomplicated malaria patients with or without previous malaria experiences. METHODS: Anti-P.falciparum IgG subclasses and IgE antibodies in plasma of complicated and uncomplicated malaria patients with or without previous malaria experiences were analysed using ELISA. IL4-590 polymorphisms were genotyped using RFLP-PCR. Statistical analyses of the IgG subclasses and IgE levels were done by Oneway ANOVA. Genotype differences were tested by Chi-squared test. RESULTS: The IL4-590T allele was significantly associated with anti-P. falciparum IgG3 antibody levels in patients with complicated (P=0.031), but not with uncomplicated malaria (P=0.622). Complicated malaria patients with previous malaria experiences carrying IL4-590TT genotype had significantly lower levels of anti-P. falciparum IgG3 (P=0.0156), while uncomplicated malaria patients with previous malaria experiences carrying the same genotype had significantly higher levels (P=0.0206) compared to their IL4-590 counterparts. The different anti-P. falciparum IgG1 and IgG3 levels among IL4-590 genotypes were observed. Complicated malaria patients with previous malaria experiences tended to have lower IgG3 levels in individuals carrying TT when compared to CT genotypes (P=0.075). In contrast, complicated malaria patients without previous malaria experiences carrying CC genotype had significantly higher anti-P. falciparum IgG1 than those carrying either CT or TT genotypes (P=0.004, P=0.002, respectively). CONCLUSIONS: The results suggest that IL4-590C or T alleles participated differently in the regulation of anti-malarial antibody isotype profiles in primary and secondary malaria infection and, therefore, could play an important role in alteration of malaria severity.

  • 106.
    Tjärnlund, Anna
    et al.
    Stockholm University, Faculty of Science, The Wenner-Gren Institute .
    Rodriguez, Ariane
    Cardona, Pere-Joan
    Guirado, Evelyn
    Ivanyi, Juraj
    Singh, Mahavir
    Troye-Blomberg, Marita
    Stockholm University, Faculty of Science, The Wenner-Gren Institute , Immunology.
    Fernandez, Carmen
    Polymeric Ig receptor knockout mice are more susceptible to mycobacteria infection in the respiratory tract2006In: International Immunology, ISSN 0953-8178, E-ISSN 1460-2377, Vol. 18, no 5, p. 807-816Article in journal (Refereed)
    Abstract [en]

    It is generally accepted that cellular, and not humoral immunity, plays the crucial role in defense against intracellular bacteria. However, accumulating data indicate the importance of humoral immunity for the defense against a number of intracellular bacteria, including mycobacteria. We have investigated the role of secretory IgA, the main isotype found in mucosal tissues, in protection against mycobacterial infection, using polymeric IgR (pIgR)-deficient mice. Characterization of the humoral response induced after intra-nasal immunizations with the mycobacterial antigen PstS-1 revealed a loss of antigen-specific IgA response in saliva from the knockout mice. IgA level in the bronchoalveolar lavage of knockout mice was similar to wild-type level, although the IgA antibodies must have reached the lumen by other means than pIgR-mediated transport. Infection with Mycobacterium bovis bacillus Calmette–Guérin (BCG) demonstrated that the immunized pIgR−/− mice were more susceptible to BCG infection than immunized wild-type mice, based on higher bacterial loads in the lungs. This was accompanied by a reduced production of both IFN-γ and tumor necrosis factor-alpha (TNF-α) in the lungs. Additionally, the pIgR−/− mice displayed reduced natural resistance to mycobacterial infection proved by significantly higher bacterial growth in their lungs compared with wild-type mice after infection with virulent Mycobacterium tuberculosis. The knockout mice appeared to have a delayed mycobacteria-induced immune response with reduced expression of protective mediators, such as IFN-γ, TNF-α, inducible nitric oxide synthase and regulated upon activation normal T cell sequence, during early infection. Collectively, our results show that actively secreted IgA plays a role in protection against mycobacterial infections in the respiratory tract, by blocking entrance of bacilli into the lungs, in addition to modulation of the mycobacteria-induced pro-inflammatory response.

  • 107.
    Tjärnlund, Anna
    et al.
    Stockholm University, Faculty of Science, The Wenner-Gren Institute , Immunology.
    Rodríguez, Ariane
    Stockholm University, Faculty of Science, The Wenner-Gren Institute .
    Cardona, P J
    Guirado, E
    Ivanyi, J
    Singh, M
    Marsh, P.D.
    Williams, A
    Troye-Blomberg, M
    Fernandez, Carmen
    Polymeric Ig receptor knockout mice are more susceptible to mycobacteria infection in the respiratory tract2006In: International Immunology, ISSN 0953-8178, E-ISSN 1460-2377, Vol. 18, no 5, p. 807-816Article in journal (Refereed)
    Abstract [en]

    It is generally accepted that cellular, and not humoral immunity, plays the crucial role in defense against intracellular bacteria. However, accumulating data indicate the importance of humoral immunity for the defense against a number of intracellular bacteria, including mycobacteria. We have investigated the role of secretory IgA, the main isotype found in mucosal tissues, in protection against mycobacterial infection, using polymeric IgR (pIgR)-deficient mice. Characterization of the humoral response induced after intra-nasal immunizations with the mycobacterial antigen PstS-1 revealed a loss of antigen-specific IgA response in saliva from the knockout mice. IgA level in the bronchoalveolar lavage of knockout mice was similar to wild-type level, although the IgA antibodies must have reached the lumen by other means than pIgR-mediated transport. Infection with Mycobacterium bovis bacillus Calmette–Guérin (BCG) demonstrated that the immunized pIgR−/− mice were more susceptible to BCG infection than immunized wild-type mice, based on higher bacterial loads in the lungs. This was accompanied by a reduced production of both IFN-γ and tumor necrosis factor-alpha (TNF-α) in the lungs. Additionally, the pIgR−/− mice displayed reduced natural resistance to mycobacterial infection proved by significantly higher bacterial growth in their lungs compared with wild-type mice after infection with virulent Mycobacterium tuberculosis. The knockout mice appeared to have a delayed mycobacteria-induced immune response with reduced expression of protective mediators, such as IFN-γ, TNF-α, inducible nitric oxide synthase and regulated upon activation normal T cell sequence, during early infection. Collectively, our results show that actively secreted IgA plays a role in protection against mycobacterial infections in the respiratory tract, by blocking entrance of bacilli into the lungs, in addition to modulation of the mycobacteria-induced pro-inflammatory response.

  • 108.
    Vafa, Manijeh
    et al.
    Stockholm University, Faculty of Science, The Wenner-Gren Institute.
    Maiga, Bakary
    Department of Epidemiology of Parasitic Diseases, Faculty of Medicine,Pharmacy and Odontostomatology, University of Bamako, Mali.
    Israelsson, Elisabeth
    Stockholm University, Faculty of Science, The Wenner-Gren Institute.
    Dolo, Amagana
    Doumbo, Ogobara K
    Troye-Blomberg, Marita
    Stockholm University, Faculty of Science, The Wenner-Gren Institute, Immunology.
    Impact of the IL-4 -590 C/T transition on the levels of Plasmodium falciparum specific IgE, IgG, IgG subclasses and total IgE in two sympatric ethnic groups living in Mali.2009In: Microbes and infection, ISSN 1286-4579, E-ISSN 1769-714X, Vol. 11, no 8-9, p. 779-84Article in journal (Refereed)
    Abstract [en]

    This study aimed to examine the effect of IL-4 -590 T/C polymorphism on the levels of malaria-specific IgE, IgG, IgG (1-4) subclasses as well as total IgE in the Fulani and their sympatric ethnic group, the Dogon, in Mali. Asymptomatic individuals, of the Fulani and the Dogon ethnic groups, were included in the study. IL-4 is involved in the regulation of IgE and IgG4 subclass. In line with this we found that within the Fulani, the T allele was associated with increased levels of total and anti-malarial IgE (P=0.02 and P=0.04, respectively). The Fulani T allele carriers had slightly higher levels of malarial specific IgG4 as compared to those with the CC genotype (P=0.08). No such differences were observed amongst the Dogon individuals. Taken together, these data indicate that the impact of IL-4 -590 variants on antibody levels may vary in different ethnic populations, and that this might affect the Ig-class and subclass distributions.

  • 109.
    Xu, Lili
    et al.
    Stockholm University, Faculty of Science, The Wenner-Gren Institute, Immunology.
    Zheng, Xiaoying
    Berzins, Klavs
    Stockholm University, Faculty of Science, The Wenner-Gren Institute, Immunology.
    Chaudhuri, Asok
    Cytokine dysregulation associated with malarial anemia in Plasmodium yoelii infected mice2013In: American Journal of Translational Research, ISSN 1943-8141, E-ISSN 1943-8141, Vol. 5, no 2, p. 235-245Article in journal (Refereed)
    Abstract [en]

    The mechanisms of malaria anemia remain incompletely understood although much effort has been put on studies in both human and murine systems. Hematopoiesis is regulated by the proliferation, differentiation and maturation of erythropoietic progenitor cells into erythrocytes and is tightly controlled by a complex communication network of cytokines as signal mediators. The present study used the murine P. yoelii 17XNL malaria model to investigate the profile of cytokines and leukocytes throughout the entire infection. Moreover, malaria induced anemia was studied in comparison with anemia induced by hemorrhage and hemolysis. During the P. yoelii infection, the levels of erythropoietic-related cytokines, such as G-CSF, GMCSF, IL-7, and IL-17, were pronouncedly reduced, while those of regulatory cytokines, such as IL-10 and TNF-alpha, were constantly increased. This cytokine profile corresponded well with the cellular composition during the infection, such as drastically decreased levels of CD4(+) and CD8(+) T cells. The profiles of erythropoiesis or hematopoiesis related cytokines during malarial anemia showed striking differences from those during anemia induced by hemorrhage or hemolysis. This study demonstrates that a markedly dysregulated cytokine network occurred in this murine malaria model, which may open a new window of insight into the mechanisms of malaria related anemia.

  • 110. Zuber, Bartek
    et al.
    Rudstrom, Karin
    Ehrnfelt, Cecilia
    Ahlborg, Niklas
    Stockholm University, Faculty of Science, The Wenner-Gren Institute, Immunology. Mabtech, Sweden.
    Epitope Mapping of Neutralizing Monoclonal Antibodies to Human Interferon-gamma Using Human-Bovine Interferon-gamma Chimeras2016In: Journal of Interferon and Cytokine Research, ISSN 1079-9907, E-ISSN 1557-7465, Vol. 36, no 9, p. 542-551Article in journal (Refereed)
    Abstract [en]

    Our aim was to identify conformational epitopes, recognized by monoclonal antibodies (mAbs) made against human (h) interferon (IFN)-. Based on the mAbs' (n=12) ability to simultaneously bind hIFN- in ELISA, 2 epitope clusters with 5mAbs in each were defined; 2mAbs recognized unique epitopes. Utilizing the mAbs' lack of reactivity with bovine (b) IFN-, epitopes were identified using 7h/bIFN- chimeras where the helical regions (A-F) or the C terminus were substituted with bIFN- residues. Chimeras had a N-terminal peptide tag enabling the analysis of mAb recognition of chimeras in ELISA. The 2mAb clusters mapped to region A and E, respectively; the epitopes of several mAbs also involved additional regions. MAbs in cluster A neutralized, to various degrees, IFN--mediated activation of human cells, in line with the involvement of region A in the IFN- receptor interaction. MAbs mapping to region E displayed a stronger neutralizing capacity although this region has not been directly implicated in the receptor interaction. The results corroborate earlier studies and provide a detailed picture of the link between the epitope specificity and neutralizing capacity of mAbs. They further demonstrate the general use of peptide-tagged chimeric proteins as a powerful and straightforward method for efficient mapping of conformational epitopes.

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