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  • 1.
    Dahle, Charlotte
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Clinical Immunology.
    Skogh, Thomas
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Östergötlands Läns Landsting, Centre for Medicine, Department of Rheumatology in Östergötland.
    Åberg, A K
    Örebro.
    Jalal, A
    Örebro.
    Olcén, Per
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Clinical Microbiology.
    Methods of choice for diagnostic antinuclear antibody (ANA) screening: Benefit of adding antigen-specific assays to immunofluorescence microscopy2004In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 22, no 3, p. 241-248Article in journal (Refereed)
    Abstract [en]

    Objectives. To evaluate and compare the performances of three enzyme-immunoassays (EIAs) and a double radial immunodiffusion (DRID) test in addition to immunofluorescence (IF) microscopy for routine laboratory screening of patient sera sent for antinuclear antibody (ANA) analysis. Methods. 3079 consecutive patient sera sent for routine testing of ANA were analysed by IF microscopy on HEp-2 cells (IF-ANA), three different ANA-EIAs, and a DRID test for antibodies against extractable nuclear antigens. The IF-ANA and DRID tests were regarded as reference methods. Results. By IF-ANA and/or DRID, 375 sera (12%) turned out ANA-positive. A further 171 sera (6%) were positive by EIA, but could not be confirmed either by IF microscopy or DRID. 32 of the 375 ANA-positive (9%) sera were negative by IF microscopy, but had precipitating antibodies against Ro/SS-A (52 and/or 60 kD). Conclusions. Different assays for ANA analysis give overlapping results to a certain extent, but are by no means interchangeable. Thus, different ANA tests reflect different aspects of these autoantibodies. The diagnostic utility of ANA testing still mainly refers to IF-microscopy and precipitin tests. IF-ANA should not be abandoned as the golden standard in clinical routine, until diagnostic and classification criteria for systemic lupus erythematosus and other systemic inflammatory autoimmune diseases have been revised. However, in addition we strongly advocate that a specific test for anti-Ro/SS-A antibodies is always included.

  • 2.
    Hellmark, Thomas
    et al.
    Lund University, Sweden .
    Segelmark, Mårten
    Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Nephrology.
    Diagnosis and classification of Goodpastures disease (anti-GBM)2014In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 48-49, p. 108-112Article in journal (Refereed)
    Abstract [en]

    Goodpastures disease or anti-glomerular basement membrane disease (anti-GBM-disease) is included among immune complex small vessel vasculitides. The definition of anti-GBM disease is a vasculitis affecting glomerular capillaries, pulmonary capillaries, or both, with GBM deposition of anti-GBM auto-antibodies. The disease is a prototype of autoimmune disease, where the patients develop auto-antibodies that bind to the basement membranes and activate the classical pathway of the complement system, which start a neutrophil dependent inflammation. The diagnosis of anti-GBM disease relies on the detection of anti-GBM antibodies in conjunction with glomerulonephritis and/or alveolitis. Overt clinical symptoms are most prominent in the glomeruli where the inflammation usually results in a severe rapidly progressive glomerulonephritis. Despite modern treatment less than one third of the patients survive with a preserved kidney function after 6 months follow-up. Frequencies vary from 0.5 to 1 cases per million inhabitants per year and there is a strong genetic linkage to HLA-DRB1*1501 and DRB1*1502. Essentially, anti-GBM disease is now a preferred term for what was earlier called Goodpastures syndrome or Goodpastures disease; anti-GBM disease is now classified as small vessel vasculitis caused by in situ immune complex formation; the diagnosis relies on the detection of anti-GBM in tissues or circulation in conjunction with alveolar or glomerular disease; therapy is effective only when detected at an early stage, making a high degree of awareness necessary to find these rare cases; 20-35% have anti-GBM and MPO-ANCA simultaneously, which necessitates testing for anti-GBM whenever acute test for ANCA is ordered in patients with renal disease.

  • 3.
    Hultman, Per
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Molecular and Immunological Pathology. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Pathology and Clinical Genetics.
    Nielsen, J
    The effect of dose, gender, and non-H-2 genes in murine mercury-induced autoimmunity2001In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 17, no 1, p. 27-37Article in journal (Refereed)
    Abstract [en]

    We have studied the effect of dose, treatment time, gender and non-H-2 genes on immune parameters and toxicokinetics in murine mercury-induced autoimmunity (HgAI). The partly-proven mechanism for HgAI is the modification of the autoantigen fibrillarin by mercury, followed by a T cell-dependent immune response driven by the modified fibrillarin. In the H-2 congenic (H-2S) mouse strains A.SW and B10.S given 203HgCl2 in a dose of 0.25-8 mg Hg/l drinking water for up to 10 weeks, the internal dose measured as the whole-body retention of mercury reached steady state within 5 weeks. Fifty percent of the steady state level was reached already after 2 days. Conditions therefore exist for a rapid modification of fibrillarin, followed by a T cell-dependent immune response, which is consistent with the presence of anti-fibrillarin antibodies (AFA) in serum after 2 weeks. AFA developed in a dose-dependent pattern. Serum IgE showed a dose-dependent increase with a maximum after 1-2.5 weeks followed by a distinct decline towards the baseline level. Substantial polyclonal B-cell activation (PBA) developed in the highest dose groups only. Since AFA developed using lower doses too, PBA can be excluded as a general mechanism for induction of AFA. Tissue immune-complex (IC) deposits were present in the highest dose groups only, indicating a possible causality between PBA and IC deposits. The substantially lower whole body and organ mercury level needed to induce AFA in the A.SW strain as compared with the H-2 congenic B10.S strain, demonstrates that genetic factors outside the H-2 region, and not related to toxicokinetics, modifies the autoimmune response. In contrast, the difference in mercury thresholds for induction of IgE was only slight between A.SW and B10.S mice, indicating basically different mechanisms for induction of AFA and serum IgE.

  • 4.
    Lundberg, K.
    et al.
    Rheumatology Unit, Department of Medicine, Karolinska Inst., Karolinska H., Stockholm, Sweden.
    Ottosson, L.
    Rheumatology Unit, Department of Medicine, Karolinska Inst., Karolinska H., Stockholm, Sweden.
    Westman, E.
    Rheumatology Unit, Department of Medicine, Karolinska Inst., Karolinska H., Stockholm, Sweden.
    Sunnerhagen, Maria
    Linköping University, The Institute of Technology. Linköping University, Department of Physics, Chemistry and Biology, Molecular Biotechnology .
    Hultenby, K.
    Pathology Unit, Karolinska Institutet, Stockholm, Sweden.
    Erlandsson, Harris H.
    Erlandsson Harris, H., Rheumatology Unit, Department of Medicine, Karolinska Inst., Karolinska H., Stockholm, Sweden.
    A pH-induced modification of CII increases its arthritogenic properties2004In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 23, no 2, p. 95-102Article in journal (Refereed)
    Abstract [en]

    Immunoreactivity to collagen type II (CII) has been implicated in the pathogenesis of rheumatoid arthritis. Patients have been described to have an acidic pH in their inflamed synovial tissue. It is known that protein structures are modified by environmental pH, thus it is plausible that changes in synovial pH could affect the conformation of proteins like CII. Posttranslational modifications could alter the biophysical properties of cartilage proteins leading to autoimmunity. In this study we investigated if arthritogenicity of CII was affected by changes in pH, and if so, this could be correlated to altered protein conformation. Immunisation with CII at neutral pH induced a milder disease than did CII at acidic pH. All animals elicited a humoral response to CII, although with a significantly higher IgG1/IgG2b-ratio in the pH 7.4 group. Analysis by circular dichroism and electron microscopy indicated less fibrillation of CII at low pH as compared to neutral pH. Our results suggest that CII is more immunogenic and arthritogenic in an acidic environment than in a neutral environment. We can correlate these findings to pH-induced conformational changes of CII. Hence, self-tolerance to CII might be affected by changes in pH leading to altered and increased arthritogenicity. © 2004 Elsevier Ltd. All rights reserved.

  • 5.
    Martinsson, Klara
    et al.
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Karlsson, Louise
    Linköping University, Department of Clinical and Experimental Medicine, Molecular and Immunological Pathology. Linköping University, Faculty of Health Sciences.
    Kleinau, Sandra
    Department of Cell and Molecular Biology, Uppsala University, Uppsala, Sweden.
    Hultman, Per
    Linköping University, Department of Clinical and Experimental Medicine, Molecular and Immunological Pathology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Diagnostics, Department of Clinical Pathology and Clinical Genetics.
    The effect of activating and inhibiting Fc-receptors on murine mercury-induced autoimmunity2008In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 31, no 1, p. 22-29Article in journal (Refereed)
    Abstract [en]

    Fc-receptors for IgG (FcgammaR) link cellular and humoral immune responses, controlling the balance between activating and inhibitory immune responses, and are involved in autoimmune diseases. Mercury (Hg) induces an autoimmune condition in genetically (H-2(s,q,f)) susceptible mice characterized by lymphoproliferation, hypergammaglobulinemia and IgG antinucleolar antibodies (ANoA). Here we investigate the role of activating (FcgammaRI, FcgammaRIII) and inhibitory (FcgammaRIIb) Fc-receptors on mercury-induced autoimmunity (HgIA) using DBA/1 mice (H-2(q)) with targeted FcgammaR mutations and wild type (wt) mice. Mice deficient for the FcRgamma-chain or FcgammaRIII and treated with 15 mg/L HgCl(2) showed a delayed and attenuated IgG1, IgG2a and IgG2b ANoA response compared to wt mice. Female Hg-treated FcgammaRIIB(-/-) mice showed a significant increased of IgG2b ANoA development compared to wt mice. The total serum IgG1 response due to Hg was attenuated in FcRgamma(-/-) and FcgammaRIII(-/-) mice compared to wt mice. Hg-treated FcgammaRIIB(-/-) mice showed an increase of both serum IgG1 and IgE compared to wt mice. We conclude that FcgammaRIII is of importance for the rapidity and final strength of the ANoA response and the increase in serum IgG1 in HgIA, while lack of FcgammaRIIb increases the IgG2b ANoA response and the serum IgG1 and IgE response.

  • 6.
    Mäkelä, Miia
    et al.
    Immunogenetics Lab, University of Turku, Finland.
    Vaarala, Outi
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Pediatrics. Östergötlands Läns Landsting, Centre of Paediatrics and Gynecology and Obstetrics, Department of Paediatrics in Linköping.
    Hermann, Robert
    Immunogenomics Lab, Cell Screen Applied Biomedi cal Res Center, Budapest. Hungary.
    Salminen, Kimmo
    Dept of Virology, Turku, Finland.
    Vahlberg, Tero
    Dept of Biostatistics University of Turku, Finland.
    Veijola, Riita
    Dept of Pediatrics, University of Oulu, Finland.
    Hyöty, Heikki
    Dept of Virology, University of Tampere, Finland.
    Knip, Mikael
    Hospital for Children and Adolescents, University of Helsinki, Finland.
    Simell, Olli
    Immunogenetics Lab, University of Turku, Finland.
    Ilonen, Jorma
    Dept of Clin Microbiology, University of Kuopio, Finland.
    Enteral virus infections in early childhood and an enhanced type 1 diabetes-associated antibody response to dietary insulin2006In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 27, no 1, p. 54-61Article in journal (Refereed)
    Abstract [en]

    Enteral virus infections may trigger the development of β-cell-specific autoimmunity by interacting with the gut-associated lymphoid system. We analyzed the effect of three different virus infections on immunization to dietary insulin in children carrying increased genetic risk for type 1 diabetes. Forty-six of 238 children developed multiple diabetes-associated autoantibodies and 31 clinical diabetes (median follow-up time 75 months). Insulin-binding antibodies were measured with EIA method (median follow-up time 24 months). Antibodies to enteroviruses, rotavirus and adenovirus were measured with EIA in samples drawn at birth and the ages of 3 and 6 months. Nineteen enterovirus, 14 rotavirus and 8 adenovirus infections were diagnosed. At the ages of 6, 12, and 18 months, the concentrations of insulin-binding antibodies were higher in children with postnatal entero-, rota- and/or adenovirus infections than in children without these infections. Children who subsequently developed ICA or IA-2 antibodies or clinical type 1 diabetes had higher concentrations of insulin-binding antibodies than children who remained autoantibody negative. Our data suggest that enteral virus infections can enhance immune response to insulin, induced primarily by bovine insulin in cow's milk. An enhanced antibody response to dietary insulin preceded the development of β-cell specific autoimmunity and type 1 diabetes. © 2006 Elsevier Ltd. All rights reserved.

  • 7.
    Nilsson, Bengt-Olof
    et al.
    Linköping University, Department of Molecular and Clinical Medicine, Infectious Diseases. Linköping University, Faculty of Health Sciences.
    Skogh, Thomas
    Linköping University, Department of Molecular and Clinical Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Rheumatology in Östergötland.
    Ernerudh, Jan
    Linköping University, Department of Molecular and Clinical Medicine, Clinical Immunology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Immunology and Transfusion Medicine.
    Johansson, Boo
    Department of Psychology, Göteborg University, Göteborg, Sweden.
    Löfgren, Sture
    Department of Microbiology, Ryhov Hospital, Jönköping, Sweden.
    Wikby, Anders
    Institute of Gerontology, School of Health Sciences, Jönköping, Sweden.
    Dahle, Charlotte
    Linköping University, Department of Molecular and Clinical Medicine, Clinical Immunology. Linköping University, Faculty of Health Sciences.
    Antinuclear antibodies in the oldest-old women and men2006In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 27, no 4, p. 281-288Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to compare the prevalence of antinuclear antibodies (ANA) in very old individuals (≥86 years of age) with healthy younger (18-68 years) blood donors (n = 200) regarding gender, health status, ratio of circulating CD4/CD8 cells and cytomegalovirus (CMV) serology. Frozen plasma was used for ANA detection in two study groups, i.e. 'OCTO' (97 persons aged 86-92 years, 65% women) and 'NONA' (136 persons aged 86-95 years, 70% women). OCTO participants were recruited on the basis that they were healthy or moderately healthy according to a selection protocol. No exclusion criteria regarding health status were applied in the NONA sample. The prevalence of ANA was significantly higher in the oldest-old samples compared to blood donors. There was no association between health status and the presence of ANA in the oldest-old. The difference across age was most pronounced in men, with low levels at younger age, whereas the prevalence among the oldest-old men reached similar levels as in women. There were no associations between the presence of ANA and CD4/CD8 ratio or with CMV status in the oldest-old. Our findings confirm an increased prevalence of ANA in the oldest-old, and emphasize the importance of taking gender and age into consideration when evaluating ANA. © 2006 Elsevier Ltd. All rights reserved.

  • 8.
    Ola, Thomas O
    et al.
    Queen Mary College, London, UK.
    Biro, Paul A
    Queen Mary College, London, UK.
    Hawa, Mohammed I
    Queen Mary College, London, UK.
    Ludvigsson, Johnny
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Pediatrics. Östergötlands Läns Landsting, Centre of Paediatrics and Gynecology and Obstetrics, Department of Paediatrics in Linköping.
    Locatelli, Matia
    Ospedale Pediatrico Bambino Gesu, Rome, Italy.
    Puglisi, Maria A
    Ospedale Pediatrico Babino Gesu, Rome, Italy.
    Bottazzo, Gian Franco
    Ospedale Pediatrico Babino Gesu, Rome, Italy.
    Fierabracci, Alessandra
    Ospedale Pediatrico Babino Gesu, Rome, Italy.
    Importin beta: A novel autoantigen in human autoimmunity identified by screening random peptide libraries on phage2006In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 26, no 3, p. 197-207Article in journal (Refereed)
    Abstract [en]

    By screening random peptide libraries (RPLs) with sera of Type 1 diabetes (T1D) patients, we previously identified 5 disease-specific 'mimotopes' displayed on phages (phagotopes). We already characterised 1 phagotope (CH1p), as an epitope of human osteopontin, an autoantigen expressed within the somatostatin cells of human islets. In this paper, we report the characterization of the second phagotope, 195Dyn, by immunohistochemistry, Western Blotting and screening of a human islet cDNA library using rabbit anti-195Dyn antibodies. The 195Dyn mimotope was detected in human islets. The screening of a λgt11 cDNA library from human islets has identified a clone, which corresponded to human importin beta. ELISA detected autoantibodies against this protein in sera of around 60% of TD1 patients and in 30% of patients affected by other autoimmune diseases. In summary, RPLs technology proved again successful in identifying another novel autoantigen (importin beta), whose significance in the autoimmune process remains to be fully elucidated. © 2006 Elsevier Ltd. All rights reserved.

  • 9.
    Pollard, Michael K
    et al.
    Scripps Research Institute, USA .
    Hultman, Per
    Linköping University, Department of Clinical and Experimental Medicine, Molecular and Immunological Pathology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Diagnostics, Department of Clinical Pathology and Clinical Genetics.
    Toomey, Christopher B.
    Scripps Research Institute, USA .
    Cauvi, David M.
    Scripps Research Institute, USA .
    Hoffman, Hal M.
    University of Calif San Diego, USA .
    Hamel, John C.
    Scripps Research Institute, USA .
    Kono, Dwight H.
    Scripps Research Institute, USA .
    Definition of IFN-gamma-related pathways critical for chemically-induced systemic autoimmunity2012In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 39, no 4, p. 323-331Article in journal (Refereed)
    Abstract [en]

    IFN-gamma is essential for idiopathic and murine mercury-induced systemic autoimmunity (mHgIA), and heterozygous IFN-gamma(+/-) mice also exhibit reduced disease. This suggests that blocking specific IFN-gamma-related pathways that may only partially inhibit IFN-gamma production or function will also suppress autoimmunity. To test this hypothesis, mice deficient in genes regulating IFN-gamma expression (Casp1, Nlrp3, Il12a, Il12b, Stat4) or function (Ifngr1, Irf1) were examined for mHgIA susceptibility. Absence of either Ifngr1 or Irf1 resulted in a striking reduction of disease, while deficiency of genes promoting IFN-gamma expression had modest to no effect. Furthermore, both Irf1- and Ifng-deficiency only modestly reduced the expansion of CD44(hi) and CD44(hi)CD55(lo) CD4(+) T cells, indicating that they are not absolutely required for T cell activation. Thus, there is substantial redundancy in genes that regulate IFN-gamma expression in contrast to those that mediate later signaling events. These findings have implications for the therapeutic targeting of IFN-gamma pathways in systemic autoimmunity.

  • 10.
    Pöntynen, Nora
    et al.
    Dept of Molecular Medicine National Public Health Institute, Helsinki, Finland.
    Miettinen, Aaro
    Dept of Bacteriology and Immunology University of Helsinki, Finland.
    Petteri Arstila, T
    Dept of Bacteriology and Immunology, University of Helsinki, Finland.
    Kämple, O
    Dept of Medical Sciences University of Uppsala, Sweden.
    Alimohammadi, Mohammad
    Dept of Medical Sciences University of Uppsala, Sweden.
    Vaarala, Outi
    National Public Health Institute, Helsinki.
    Peltonen, Leena
    Dept of Molecular Medicine National Public Health Institute, Helsinki, Finland.
    Ulmanen, Ismo
    Dept of Molecular Medicine National Public Health Institute, Helsinki, Finland.
    Aire deficient mice do not develop the same profile of tissue-specific autoantibodies as APECED patients2006In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 27, no 2, p. 96-104Article in journal (Refereed)
    Abstract [en]

    Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED, or APS1), is a monogenic autoimmune disease caused by mutations in the autoimmune regulator (AIRE) gene. The three main components of APECED are chronic mucocuteaneous candidiasis, hypoparathyroidism and adrenocortical insufficiency. However, several additional endocrine or other autoimmune disease components, or ectodermal dystrophies form the individually variable clinical picture of APECED. An important feature of APECED is a spectrum of well-characterized circulating autoantibodies, reacting against tissue-specific autoantigens. Aire deficient mice develop some characteristics of APECED phenotype. In order to investigate whether the Aire deficient mice produce autoantibodies similar to human APECED, we studied the reactivity of Aire mouse sera against mouse homologues of 11 human APECED antigens. None of the APECED antigens indicated elevated reactivity in the Aire knock-out mouse sera, implying the absence of APECED associated autoantibodies in Aire deficient mice. These findings were supported by the failure of the autoantigens to activate mouse T-cells. Furthermore, Aire knock-out mice did not express increased levels of anti-nuclear antibodies compared to wt mice. This study indicates that spontaneous induction of tissue-specific autoantibodies similar to APECED does not occur in the rodent model suggesting differences in the immunopathogenic mechanisms between mice and men.

  • 11. Schloot, N
    et al.
    Meierhoff, G
    Karlsson Faresjö, Maria
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Pediatrics.
    Ott, Patrick
    Putnam, A
    Lehman, P
    Gottlieb, P
    Roep, BO
    Peakman, M
    Tree, T
    Comparison of cytokine ELISpot assay formats for the detection of islet antigen autoreactive T cells: Report of the third immunology of diabetes society T-cell workshop2003In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 21, no 4, p. 365-376Article in journal (Refereed)
    Abstract [en]

    The identification of sensitive assay formats capable of distinguishing islet autoreactive T cells directly ex vivo in blood is a major goal in type 1 diabetes research. Recently, much interest has been shown in the cytokine enzyme linked immunospot assay (CK ELISpot), an assay potentially capable of fulfilling these difficult criteria. To address the utility of this assay in detecting autoreactive T cells, a 'wet' workshop was organized using the same fresh blood sample and coded antigens. Five different laboratories participated, using three distinct CK ELISpot assay formats. Samples from two subjects were pre-tested for responses to sub-optimal concentrations of tetanus toxoid, representing a low frequency recall response, and peptides from diabetes associated autoantigens GAD65, IA-2 and HSP60. All participants measured interferon-? production and combinations of interleukins-4, -5, -10 and -13. In the workshop 4 of 5 laboratories detected low frequency recall responses in both subjects and 3 of 5 detected at least one of the autoreactive peptide responses concordant with pre-testing. Significant assay format related differences in sensitivity and signal-to-noise ratio were observed. The results demonstrate the potential for detection of low-level autoreactive T cell responses and identify assay characteristics that will be useful for studies in type 1 diabetes. ⌐ 2003 Elsevier Ltd. All rights reserved.

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