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Dermal Hypersensitivity: Immunologic Principles and Current Methods of Assessment
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
In the U.S. the five most common causes of ACD have been reported to be Toxicodendron (Rhus) plant resin (urushiol from poison ivy, poison oak, and poison sumac), nickel, paraphenyldiamine, rubber compounds, and ethylenediamine.14 It is estimated that 50 to 70% of the American population are sensitized to Toxicodendron and would react positively to provocative testing, while about 30% are assumed to have an antigen-specific genetic tolerance to this contact sensitizer.15 The Compositae family of plants, especially the genera Ambrosia and Chrysanthemum, are other common plant contact sensitizers, due principally to the presence of sesquiterpene lactones.16 Many other contact sensitizers are chemicals which act as haptens, or incomplete antigens with low molecular weights that bind to macromolecules in the body to become allergenic.
Historical perspectives of allergen immunotherapy
Published in Richard F. Lockey, Dennis K. Ledford, Allergens and Allergen Immunotherapy, 2020
David Fitzhugh, Sheldon G. Cohen, Richard Evans
The first move to explain the procedure that originated in folk medicine in terms of immune phenomena began with the approach of Strickler in 1918. Although unable to demonstrate circulating blood antibodies in patients affected by poison ivy and poison oak dermatitis, Strickler postulated the likely pathogenesis to be a form of “tissue immunity” to the plant toxins. Believing the mechanism to be similar to that of hay fever, he introduced adaptation of desensitization for treatment and prevention of the plant-related contact dermatitis with extracts of the alcohol-soluble leaf fraction given by intramuscular injection [137]. The following year, Schamberg introduced an oral approach to prophylactic desensitization using incremental drop doses of a tincture of Rhus toxicodendron [138]. Strickler's follow-up report 3 years later indicated favorable acceptance of intramuscular injection, oral methods, and a combination of both [134]. Although trials during subsequent years supported this early usage [139], there were differing reports varying from only short-term immunizing effects [140] to lack of either clinical benefit [141] or increased tolerance [142].
Antigens
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Haptens may complex with self proteins in vivo under certain circumstances, and generate new T cell epitopes. For example, non-immunogenic chemicals may react with components of skin, creating new immunogenic structures. A vigorous immune response to these new antigens results in a contact hypersensitivity reaction (see Chapter 6). An example of this is the catechol derivative urushiol found in certain plants of the genus Toxicodendron, more affectionately known as poison ivy.
Himalayan poisonous plants for traditional healings and protection from viral attack: a comprehensive review
Published in Toxin Reviews, 2022
Shriya Pathania, Diksha Pathania, Priyanka Chauhan, Mamta Sharma
Hay fever caused by pollen from ragweed, birch, hazel, timothy grass, and ryegrass is the common case of phytoallergy. Urticaria resulting from eating strawberries and allergy to peanuts are some other recognized allergy conditions due to phytoconstituents. Some phytoconstituents cause certain forms of extrinsic allergic alveolitis. Pyrethrum allergy is a known problem on the plantations of Chrysanthemum cineriaefolium in many countries. The Japanese cedar (Cryptomeria japonica) is a source of annual misery because of the massive amounts of highly allergenic pollen every spring (Wink and Van Wyk 2008). A Phytoallergic problem has increased greatly in recent decades. A different allergic mechanism occurs in regions with poison ivy (Rhus toxicodendron, T. rydbergii), poison oak (Rhus juglandifolia) and poison sumac (Rhus vernix). The active ingredient is urushiol. Its first exposer of sap to the skin has no noticeable clinical effect. Urushiol acts as a hapten, however. It binds to proteins in the skin, creating new epitopes. Upon subsequent contact pronounced pruritic dermatitis develops (Wink 2010).
Bioactivation of herbal constituents: mechanisms and toxicological relevance
Published in Drug Metabolism Reviews, 2019
Urushiol (Figure 11(h)), a pale-yellow oily mixture of catechols with an alkyl side chain, are the allergenic components of Toxicodendron radicans (poison ivy) and Toxicodendron diversilobum (poison oak). Brushing up against these plants results in allergic contact dermatitis, leading to an itchy rash. Oxidation of urushiols to ortho-quinones likely results in depletion of intracellular GSH and covalent modification of macromolecules leading to skin toxicity (Dunn et al. 1982). Urushiol-induced contact dermatitis is known to be mediated by T lymphocytes that recognize urushiol-bound proteins as an antigen (Dunn et al. 1982). Urushiol ortho-quinones and/or ROS production are likely also responsible for the DNA fragmentation observed in human cancer cells treated with urushiol leading to induction of apoptosis (Kim et al. 2013).
Phytodermatitis in East and southeast of Turkey: A prospective study
Published in Cutaneous and Ocular Toxicology, 2019
ACD, another phytodermatitis due to plants, develops frequently in the USA due to toxic ivy of the toxicodendron species14. In a study by Uce Ozkol et al conducted in eastern Turkey, ACD occured in two patients due to Eryngium billardieri belonging to Apiaceae family2. There were no ACD cases due to toxicodendron species in our study. In our study, ACD developed in two patients due to X. strumarium belonging to Asteraceae family (Figure 2). Guin identified ACD cases in one or more localized areas due to Xanthium species. This reaction is due to sesquiterpene lactone, the major allergic component found in the extracts of the plants4.