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  • 1
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 292 (1981), S. 627-629 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Recent competitive antibody-binding studies using six monoclonal antibodies against different determinants on the H-2Kk molecule3 have provided information on the steric relationship of individual determinants2. The six H-2Kk determinants defined by monoclonal antibodies are concentrated on the ...
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Eosinophilia-myalgia syndrome ; L-tryptophan ; Neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In October of 1989, a clustering of cases with eosinophilia lead to the identification of a new syndrome: The eosinophilia myalgia syndrome associated with the use of an L-tryptophan product. Two years before the possible causal relationship between the use of L-tryptophan and the syndrome was described, we treated a patient with eosinophilia, severe neuropathy and disabling myopathy. Immunosuppressive therapy was required to treat the first flare of her disease. With reexposure to L-tryptophan, she relapsed and recovered when L-tryptophan was discontinued. Interestingly, she tolerated a third exposure to L-tryptophan without clinical or laboratory evidence for EMS
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  • 3
    ISSN: 1432-1440
    Keywords: Key words Autoimmunity ; T cell receptor ; Vasculitis ; Giant cell arteritis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The objective of this study was to explore the nature of the antigen-specific T cell response in giant cell arteritis by analyzing clonally expanded T cells in temporal artery specimens. In temporal artery tissue from eight patients, 10% of the T cell receptor β chain repertoire was systematically screened for clonal T cells by reverse-transcriptase polymerase chain reaction with selected BV, BJ, and BC specific primers and by direct sequencing of the amplified product. In five additional patients tissue-derived T cell clones were characterized. All expanded clonotypes were analyzed for their presence at different sites of the inflamed artery. T cell lines were tested for their proliferation to autologous monocytes pulsed with temporal artery extracts from patients with giant cell arteritis, polymyalgia rheumatica, and unrelated diseases. Clonally expanded T cells were identified in 30% of the BV-J combinations of the sampled repertoire. A subset of these clones were encountered at different sites of the inflammation, but not in the peripheral blood. The T cell receptor β chain sequences were diverse. The patients had between none and five such clonotypes in the sampled repertoire, suggesting that only few T cell specificities in each patient are involved in antigen recognition. One of these T cell clonotypes was shown to proliferate in response to an antigen selectively expressed in temporal artery specimens from giant cell arteritis and from polymyalgia rheumatica patients. Clonotypes with identical T cell receptor β chain sequences can be found at distinct sites of the inflammation in giant cell arteritis, suggesting recognition of the same antigen at different locations. At least for some of these T cell clones the antigen is shared between different giant cell arteritis and polymyalgia rheumatica patients but not expressed in temporal arteries of patients with unrelated diseases. While different HLA-DR4+ patients utilize distinct T cell specificities, the actual number of responding T cells in individual patients is small and may be disease limiting.
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 75 (1997), S. 772-785 
    ISSN: 1432-1440
    Keywords: Key words Rheumatoid arthritis ; Pathogenesis ; T cells ; HLA ; Genetic susceptibility
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Rheumatoid arthritis (RA) is an inflammatory disease targeting the synovial membrane and extra-articular tissues. The most feared consequences are significant levels of pain, functional disability, and rheumatoid organ involvement. Molecular investigations of RA have markedly changed the understanding of the pathogenesis although the etiology remains unresolved. Despite the failure of intense efforts to confirm the presence of an infectious micro-organism in rheumatoid synovium, the concept that RA is infectious in origin has continued to be attractive. Theories on the autoimmune nature of RA have benefited from the enormous progress made in understanding the cellular and molecular components of normal immune responses. However, convincing experimental evidence of a joint-specific endogenous antigen in the synovial lesions is still lacking. The viewpoint that RA represents the sequelae of systemic lymphoproliferation has recently been supported by the finding of autoreactive T cells with atypical growth and differentiation behavior. Significant cross-fertilization for the understanding of RA can be expected by studies elucidating cell cycle control and the role of proto-oncogenes. The realization that RA is a genetic disease has had and will have a major impact on investigating pathological events. As in other common genetic disorders, multiple genetic determinants contribute to the risk of an individual developing chronic inflammatory rheumatoid synovitis. Individual genetic elements are seldom mutated or abnormal, but a risk threshold is reached by their accumulation and combination. Genes encoded in the HLA region are recognized as RA risk genes. Recent studies have emphasized that a gene dosing effect for RA-associated HLA alleles is functional, and that HLA polymorphisms act as progression factors rather than as initiation factors in the disease process. These data have challenged the traditional paradigm that disease-associated HLA molecules function solely through their capability to select, bind, and present an arthritogenic antigen. Current efforts focus on identifying the spectrum and nature of genes associated with various RA phenotypes. The future will likely see a broadening of biological systems involved in the pathogenesis of RA with anomalies other than immunoresponsiveness contributing to mechanisms driving articular and extra-articular RA.
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  • 5
    ISSN: 1437-160X
    Keywords: Interferon gamma ; Rheumatoid arthritis ; Controlled clinical trial ; Multicenter
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The controlled clinical trial reported here is part of a multicenter clinical and basic research project, sponsored by the German Federal Minister of Science and Technology, directed by a standing commission of the president of the Max-Planck-Gesellschaft, and coordinated by the Max-Planck-Institut für Biochemie, München. Overall, 249 patients with rheumatoid arthritis (RA) were enrolled by 16 participating hospitals. In addition to NSAID treatment, patients were randomly given either interferon gamma (IFN-γ) or placebo. In the IFN-γ group, 107 patients were evaluated and in the control group, 116 patients were evaluated. The response rate after 3 months of treatment, according to joint pain indexes, was significantly higher in the IFN-γ group with an error probability of 1%. IFN-γ was able to reduce the quantity of corticosteroids administered. Compared with the control group, the IFN-γ group benefited considering all parameters measured. Most important side effects were transient fever and transient influenza-like symptoms; all other adverse events were comparable in both groups.
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