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Contact Hypersensitivity Reactions (contact + hypersensitivity_reaction)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Allergic contact dermatitis: the cellular effectors

CONTACT DERMATITIS, Issue 1 2002
Ian Kimber
Contact hypersensitivity reactions are mediated by lymphocytic effector cells. Until recently it was believed that the most important of these were CD4+ T lymphocytes. However, there is growing evidence that in many instances the predominant effector cell may be a CD8+ T lymphocyte, with in some instances CD4+ cells performing a counter-regulatory function. Here we review the roles of CD4+ T helper (Th) cells and CD8+ T cytotoxic (Tc) cells, and their main functional subpopulations (respectively, Th1 and Th2 cells and Tc1 and Tc2 cells) in the elicitation of contact hypersensitivity reactions and consider the implications of effector cell selectivity for the biology of allergic contact dermatitis. [source]

P73 The magnitude of contact allergy responses can be quantified with imaged perfusion

CONTACT DERMATITIS, Issue 3 2004
Bolli Bjarnason
Objective:, The objective of this study was to determine whether the magnitude of the perfusion of the contact hypersensitivity response as measured by the laser Doppler perfusion imaging (LDPI) technique was associated with immunological parameters implicated in the pathogenesis of the disease. Methods:, Urushiol was applied on one of the forearms of volunteers for 48 hours while the other forearm served as a control. Twenty-four hours later, measurements of perfusion of the patch test sites were performed with the LDPI technique. To determine whether there was a correlation with immunological parameters associated with human contact hypersensitivity, suction blisters were produced at the test sites. Blister fluid was removed and examined for the cytokine interleukin-8 (IL-8). Results:, There was an extremely close correlation between the magnitude of the contact hypersensitivity response as measured by the imaged perfusion and the level of IL-8 in the blister fluid (r = 1.00). Compared to subjects with visually positive urushiol reactions, patients who failed to develop urushiol contact hypersensitivity despite repeated exposures to that substance had both greatly diminished perfusion and blister fluid IL-8 levels. Conclusion:, The results indicate that LDPI is a sensitive method of quantifying contact hypersensitivity reactions in humans and that the magnitude of the measurements with this technique correlates extremely well with cutaneous cytokine levels that have been implicated in the immunopathogenesis of contact hypersensitivity. [source]

Allergic contact dermatitis: the cellular effectors

CONTACT DERMATITIS, Issue 1 2002
Ian Kimber
Contact hypersensitivity reactions are mediated by lymphocytic effector cells. Until recently it was believed that the most important of these were CD4+ T lymphocytes. However, there is growing evidence that in many instances the predominant effector cell may be a CD8+ T lymphocyte, with in some instances CD4+ cells performing a counter-regulatory function. Here we review the roles of CD4+ T helper (Th) cells and CD8+ T cytotoxic (Tc) cells, and their main functional subpopulations (respectively, Th1 and Th2 cells and Tc1 and Tc2 cells) in the elicitation of contact hypersensitivity reactions and consider the implications of effector cell selectivity for the biology of allergic contact dermatitis. [source]

CD4+CD25+ regulatory T cells suppress contact hypersensitivity reactions by blocking influx of effector T cells into inflamed tissue

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 11 2006
Sabine Ring Dr.
Abstract CD4+CD25+ regulatory T cells (Treg) exert suppressive functions on effector T cells in vitro and in vivo. However, the exact cellular events that mediate this inhibitory action remain largely unclear. To elucidate these events, we used intravital microscopy in a model of contact hypersensitivity (CHS) and visualized the leukocyte-endothelium interaction at the site of antigen challenge in awake C57BL/6 mice. Injection of Treg i.v. into sensitized mice at the time of local hapten challenge significantly inhibited rolling and adhesion of endogenous leukocytes to the endothelium. A similar inhibition of leukocyte recruitment could be recorded after injection of Treg-derived tissue culture supernatant. Thus, these data indicate that soluble factors may account for the suppressive effects. Accordingly we found that IL-10, but not TGF-,, was produced by Treg upon stimulation and that addition of anti-IL-10 antibodies abrogated the suppressive effects of Treg and tissue culture supernatant in CHS reactions. Moreover, CD4+CD25+ T cells isolated from IL-10,/, mice were not able to suppress the immune response induced by hapten treatment in C57BL/6 mice. In conclusion, our data suggest that cytokine-dependent rather than cell-cell contact-dependent mechanisms play a pivotal role in the suppression of CHS reactions by Treg in vivo. [source]