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Results for “Dermatitis, Toxicodendron”

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At least 37 records · Page 2Linked to original sources
PubMed1988

Urushiol (poison ivy)-triggered suppressor T cell clone generated from peripheral blood.

Allergic contact dermatitis to Toxicodendron radicans (poison ivy) is mediated by the hapten urushiol. An urushiol-specific, interleukin 2 (IL-2)-dependent T cell clone (RLB9-7) was generated from the peripheral blood of a patient with a history of allergic contact dermatitis to T. radicans. This clone proliferated specifically to both leaf extract and pure urushiol. Although the clone had the phenotype CD3+CD4+CD8+, proliferation to antigen was blocked by anti-CD8 and anti-HLA-A, B, C, but not by anti-CD4, suggesting that CD4 was not functionally associated with the T cell receptor. Furthermore, studies with antigen-presenting cells from MHC-typed donors indicated that the clone was MHC class 1 restricted. RLB9-7 was WT31 positive, indicating it bears the alpha beta T cell receptor. The clone lacked significant natural killer cell activity and produced only low levels of IL-2 or gamma-interferon upon antigen stimulation. Addition of RLB9-7 to autologous peripheral blood mononuclear cells in the presence of urushiol inhibited the pokeweed mitogen-driven IgG synthesis. This suppression was resistant to irradiation (2,000 rad) and was not seen when RLB9-7 was added to allogeneic cells, even in the presence of irradiated autologous antigen-presenting cells, suggesting that suppression was MHC restricted and not mediated by nonspecific soluble factors. However, RLB9-7 cells in the presence of urushiol inhibited the synthesis of tetanus toxoid-specific IgG by autologous lymphocytes, indicating that the suppression, although triggered specifically by urushiol, was nonspecific.

Antibody Specificity↗
PubMed2003

Clinical and immunologic features of systemic contact dermatitis from ingestion of Rhus (Toxicodendron).

Oral or parenteral exposure to certain contact allergens may elicit an eczematous skin reaction in sensitized individuals. This phenomenon has been called systemic contact dermatitis (SCD) and is relatively rare when compared with classical contact dermatitis. We reviewed and analysed the clinical and immunologic features of 42 patients with SCD caused by ingestion of Rhus (Toxicodendron), 24 males and 18 females, average age 44 years (range 24-72). Several of such patients (33%) had a known history of allergy to lacquer. The patients developed skin lesions such as generalized maculopapular eruptions (50%), erythroderma (29%), vesiculobullous lesions (14%) and erythema multiform (EM)-like lesions (7%). Many patients (57%) developed leucocytosis with neutrophilia (74%). In some patients (5%), abnormalities of liver function developed. We also analysed lymphocyte subsets in the peripheral blood of 12 patients. The lymphocyte subsets studied were T cells (CD3), B cells (CD19), natural killer (NK) cells (CD3-CD16+/CD56+), helper/inducer cells (CD4), cytotoxic/suppressor cells (CD8) and helper/suppressor ratio (CD4/CD8). The lymphocyte subsets of all 12 patients studied were within the normal range. Moreover, there were no differences between patients with a history of allergy to lacquer and those without a history of allergy to lacquer. Therefore, rather than an immunologic response, the skin eruption seems to be caused by a toxic reaction because of Rhus.

Administration, Oral↗