Contact sensitization

S., Demchuk, E. Structure-activity models for contact sensitization. Chem. Res. Toxicol. 2005, 18, 954-969. 

Animal experimental models of nickel-induced skin sensitivity are few and have been conducted only under very specialized conditions (USEPA 1986). Studies examining the mechanism of nickel contact sensitization and its extent in wildlife are needed (USPHS 1993). The importance of the surface properties and crystalline structure of nickel compounds in relation to their reactivity and protein-binding activities is well documented. It is therefore necessary to identify clearly the nickel compounds to which exposure occurs (Sunderman etal. 1984). Acute and chronic dermal and... 

Coutant, K.D. et al., Early changes in murine epidermal cell phenotype by contact sensitizers, Toxicol. ScL, 48, 74, 1999. 

Degwert, J.S., Hoppe, U. and Kligman, L. H., In vitro model for contact sensitization I. Stimulatory capacities of human blood-derived dendritic cells and their phenotypical alterations in the presence of contact sensitizers, Toxicol, in Vitro, 11,613, 1997. 

Aiba, S. et al, In vitro treatment of human transforming growth factor-betal-treated monocyte-derived dendritic cells with haptens can induce the phenotypic and functional changes similar to epidermal Langerhans cells in the initiation phase of allergic contact sensitivity reaction, Immunology, 101, 68, 2000. 

Arrighi, J.F.et al., A critical role for p38 mitogen-activated protein kinase in the maturation of human blood-derived dendritic cells induced by lipopolysaccharide, TNF-alpha, and contact sensitizers. J. Immunol., 166, 3837, 2001. 

Kripke, M. L. et al., Evidence that cutaneous antigen-presenting cells migrate to regional lymph nodes during contact sensitization, J. Immunol. 145, 2833-2838, 1990. 

Wahlberg, J. and Boman, A., Contact sensitivity to arsenical compounds. Clinical and experimental studies, Derm. Beruf. Umwelt., 34, 10, 1986. 

Sailstad, D.M., et al., A murine model for low molecular weight chemicals Differentiation of respiratory sensitizers (TMA) from contact sensitizers (DNFB), Toxicology, 194, 147, 2003. 

Antonopoulos, C., et al., Functional caspase-1 is required for Langerhans cell migration and optimal contact sensitization in mice. J. Immuno.,1 166, 3672, 2001. 

Kondo, S., Mackenzie, R.C., and Sauder, D.N., Interleukin-10 inhibits the elicitation phase of allergic contact sensitivity. J. Invest. Dermatol., 103, 811, 1994. 

In summary, chemical contact sensitization will be favored by the selective activation of Thl and Tel cells, whereas immediate type hypersensitivity reactions such as chemical respiratory hypersensitivity are apparently associated with the preferential activation of Th2 (and possibly Tc2) type cells. 

Kimber, I. and Dearman, R J., Investigation of lymph node cell proliferation as a possible immunological correlate of contact sensitizing potential. Fd Chem. Toxicol., 29, 125, 1991. 

Gerberick, G.F. et al., Examination of the local lymph node assay for use in contact sensitization risk assessment, Fundam. Appl. Toxicol., 19, 438, 1992. 

Van Och, F.M.M. et al., Cytokine production induced by low molecular weight chemicals as a function of the stimulation index in a modified local lymph node assay An approach to discriminate contact sensitizers from respiratory sensitizers. Toxicol. Appl. Pharmacol., 184,46,2002. 

For in vitro testing of nickel contact sensitivity, the lymphocyte transformation test and leucocyte migration inhibition test have been used [370]. 

Topical formulations are another special case. Over time, it has been shown that the minipig has a skin structure that is quite similar to humans, and that species is now used commonly as the nonrodent model. These types of formulations also require local irritation studies where guinea pigs are used to determine delayed contact sensitization. Selection of the animal species for the nonclinical program is often not straightforward. 

Immune Regulatory Mechanisms in Allergic Contact Dermatitis and Contact Sensitization... 

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