Analysis of the phenotype and cytokine pattern of blood- and skin-derived nickel specific T cells in allergic contact dermatitis.
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Biomedical subjects
Publications and source records attributed to A Kapp.
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Increased numbers of eosinophils in the peripheral blood and inflammatory tissue are characteristic features of allergic diseases such as allergic asthma, rhinoconjunctivitis, and atopic dermatitis. Tissue damage and propagation of inflammation is thought to be mediated by the interaction among Th2-like T cells, antigen-presenting cells, and eosinophils. In this process eosinophils are activated by several inflammatory mediators, leading to the influx of eosinophils at sites of inflammation and to tissue damage by the release of reactive oxygen species and toxic granule proteins. Therefore, agents that would be able to inhibit or antagonize mediator-induced eosinophil activation seem to be possibilities as new therapeutic strategies. In this review we will focus on the modulation of human eosinophil effector functions by monoclonal antibodies and chemokine receptor antagonists. We will discuss whether modulation of eosinophil effector functions might be successful as a possible future strategy of diseases that are accompanied by activated eosinophils. Even when these compounds show antagonistic effects on human eosinophils, in vitro future studies will be necessary to investigate whether chemokine receptor antagonists and monoclonal antibodies are suitable in vivo in an animal model prior to studies in humans.
Eosinophils are predominant effector cells in allergic and autoimmune diseases attracted by several chemokines into the inflammatory tissue. In the past many new biologically active chemokines have been cloned exploring the gnomic DNA sequence data base in the vicinity of already-known chemokine sequences. This article will help to better understand the chemokine network in eosinophil activation according to the new nomenclature of chemokines. Moreover, possible new therapies, such as chemokine receptor antagonists, for the treatment of allergies are discussed.
Different kinds of mediators, particularly chemokines, are responsible for the attraction and activation of eosinophils to the site of inflammation. In the last decade, this new family of chemotactic cytokines have become interesting because of their restricted target cell specificity. This article focuses on the activation of eosinophil effector functions in response to different CC chemokines.
Chronic urticaria (CU) involves release of histamine from mast cells and/or basophils, which in turn promotes the classic inflammatory cascade. The resultant symptoms can severely impact sufferers' quality of life and in severe cases prevent them from leading a normal existence, with consequent burdens on family and society. Rapid initiation of effective reliable therapy is important in combating CU, together with avoidance of triggers or exacerbating factors, if known. While newer immunologically-based therapies are beginning to be developed, antihistamines remain a cornerstone of effective therapy. Treatment should be tailored to individual patient circumstances, but in principle the choice of antihistamine component should be governed by the availability of evidence of rapid and prolonged efficacy specifically in CU and evidence of good tolerability and safety. Increasingly, evidence of beneficial effects on patient quality of life is also required for rational selection of an antihistamine from amongst those available. Levocetirizine is a new single-isomer antihistamine with a proven efficacy on chronic urticaria as documented in two recent clinical studies, which have included effectiveness and quality of life assessments.
Using a new C3a-radioimmunoassay, we could show a significantly increased complement activity in patients with active rheumatoid arthritis. The C3a-plasma level in rheumatoid patients was 529 ng/ml, whereas in patients with psoriatic arthropathy it was 164 ng/ml, in patients with noninflammatory muscular pain syndromes 170 ng/ml and in healthy blood donors we found a mean level of 221 ng/ml. The reproducibility was high, therefore it seems that the possibility to calculate the risks of complement-activating immunological disorders can be increased by using the C3a-radioimmunoassay. On the other hand the C3a-increase in rheumatoid patients may be an expression of the immunological activity of the disease.