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Poison oak urushiol causes a complicated delayed allergic reaction with the body's immune system. It is technically classified as a cell-mediated immune response and the "peak misery" may not appear until days or weeks later. It is quite different from the primary irritants of nettle and euphorbias, the effects of which are immediate.
The following hypothetical "two-phase" scenario for poison oak dermatitis is summarized from Epstein (1984). PHASE I (Induction): Initial contact with poison oak may result in urushiol penetrating the stratified squamous epithelial cells of the skin and binding to large dendritic (branched) white blood cells in the epidermis called Langerhan's cells. See Figure 4 below.
The Langerhan's cell (with urushiol allergen and MHC protein on its membrane) migrates to a nearby lymph node where clones of special white blood cells, called effector T-cells, are programmed to recognize urushiol. [Note: Some immunology textbooks refer to these clones of T-cells, with urushiol receptor sites on their membranes, as "helper T-cells." There are literally millions of effector T-cells (helper T-cells) roaming throughout the blood and lymphatic system, each with special receptor molecules on their membranes for a particular allergenic chemical, such as the urushiol of poison oak. T-cells patrol our circulatory system looking for invading cells and viruses, inspecting surface membranes like security guards checking I.D. cards.
PHASE II (Elicitation): If you get urushiol absorbed into the skin during a subsequent encounter with poison oak, an effector T-cell may encounter it bound to a Langerhan's cell and attach to it by a complicated and specific recognition system. The effector T-cell then produces more clones of itself and releases special proteins called lymphokines (cytokines) which attract a legion of different white blood cells, including "cell engulfing" macrophages and cytotoxic ("killer") T-cells. The killer T-cells are also produced in regional lymph nodes during the Elicitation phase, and according to some textbooks, they also have urushiol receptors on their membranes. The new army of white blood cells releases lytic enzymes and protein toxins (perforins) which destroy everything in the vicinity including membrane-bound urushiol and other skin cells, thus producing a blistering rash. Fluid oozes from the blood vessels and lymphatics (edema) and cell death and necrosis (breakdown) of skin tissue occurs. Milder effects range from redness (vasodilation) and itching (nerve injury) to small blisters (vesicles and bullae).
J Altern Complement Med. 2005 Aug;11(4):709-10.
Successful treatment of poison oak dermatitis treated with Grindelia spp. (Gumweed).
Canavan D, Yarnell E.
Bandon, OR, USA.
Poison oak and related hypersensitivity dermatitides are age-old problems that have historically been treated with herbal medicines before the availability of corticosteroids. Few of these historical therapies have been rigorously investigated. The case presented here provides some insight into the potential efficacy of certain herbs for relieving mild-to-moderate poison ivy dermatitis.
Contact Dermatitis. 2003 May;48(5):251-4.
Clinical and immunologic features of systemic contact dermatitis from ingestion of Rhus (Toxicodendron).
Oh SH, Haw CR, Lee MH.
Department of Dermatology, College of Medicine, Kyunghee University, Seoul, Korea.
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.