Contact hypersensitivity—

KATIYAR s K, ELMETS c A, AGARWAL R and MUKHTAR H (1995) Protection against ultraviolet-B radiation-induced local and systemic suppression of contact hypersensitivity and edema responses in C3H/HeN mice by green tea polyphenols , Photochem Photobiol, 62, 855-61. 

Reeve, V.E. et al.. Suppressive effect of 2-acetyl-4-tetrahydroxybutylimidazole on contact hypersensitivity in the Skh HR hairless mouse, Int. Arch. Allergy Immunol, 102, 101, 1993. 

Immunoenhancement, which, as adverse effect, may lead to immune-mediated diseases such as hypersensitivity reactions and autoimmune diseases. Hypersensitivity reactions are the result of normally beneficial immune responses acting inappropriately, causing inflammatory reactions and tissue damage. The two most frequent manifestation of chemical-induced allergy are contact hypersensitivity and respiratory sensitization, both of which can have a serious impact on quality of life and represent a common occupational health problem. Hypersensitivity reactions are often considered to be increased at such a rate to become a major health problem in relation to environmental chemical exposure. 

Maurer, T., Guinea pig predictive tests, in Toxicology of contact hypersensitivity, I. Kimber, I. and Maurer, T., Eds., Taylor Francis, London, 1996, pp 107-126. 

Lasch-Loquire and coworkers [45] evaluated the contact hypersensitivity reaction against picryl chloride (0.5 mg/Kg Pb s.c.) in mice with Pb administered just before or during the sensitization period. Pb exposure suppressed the DTH response regardless of the window (before or during sensitization) in which it had been administered. 

Schwarz, A., et al., In vivo effects of interleukin-10 on contact hypersensitivity and de-layed-type hypersensitivity reactions, J. Invest. Dermatol., 103, 211, 1994. 

Walker, D., et. al., Persistent suppression of contact hypersensitivity and altered T cell parameters in F344 rats exposed perinatally to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), Toxicology, 197, 57, 2004. 

In addition to tumor immunity, UV exposure was found to impair antigen presenting cell function, the generation of contact hypersensitivity (CHS) to chemical haptens and... 

Moodycliffe, A. M. et al., Differential effects of a monoclonal antibody to cis-urocanic acid on the suppression of delayed and contact hypersensitivity following ultraviolet irradiation, J. Immunol. 157, 2891-2899, 1996. 

El-Ghorr, A. A. and Norval, M., A monoclonal antibody to cis-urocanic acid prevents the UV-induced changes in Langerhans cells and DTH responses in mice, although not preventing dendritic cell accumulation in lymph nodes draining the site of irradiation and contact hypersensitivity responses, J. Invest. Dermatol. 105, 264-268, 1995. 

Toews, G. B., Bergstresser, R R., and Streilein, J. W., Epidermal Langerhans cell density determines whether contact hypersensitivity or unresponsiveness follows skin painting with DNFB, J. Immunol. 124, 445 449, 1980. 

Hart, P. H.et al., Histamine involvement in UVB-and cis-urocanic acid-induced systemic suppression of contact hypersensitivity responses, Immunology 91, 601-608, 1997. 

Shimizu, T., Munn, C. G., and Streilein, J. W., Transepidermal induction of contact hypersensitivity in mice with a water-soluble hapten, J. Invest. Dermatol. 101, 749-753, 1993. 

Patterson, R. et al., Arsenic-induced alterations in the contact hypersensitivity response in Balb/c mice, Toxicol. Appl. Pharmacol., 198, 434, 2004. 

The elicitation of a contact hypersensitivity response occurs when a sensitized individual is re-exposed to the antigen. The initial steps are identical to those in the... 

Exposure conditions appear to play the most important role in the induction and elicitation of contact hypersensitivity. These conditions involve factors inherent to the individual, including thickness of the exposed skin and skin condition at the exposure site. External factors including the vehicle, occlusive or non-occlusive conditions, temperature and humidity, and exposure to sunlight may also influence the development of contact allergy. 

For effective sensitization, a chemical must therefore be inherently protein-reactive or must be converted in the skin to a protein-reactive metabolite. Chemicals that are unable to associate effectively with proteins will fail to stimulate a cutaneous immune response. For those chemical contact allergens that require metabolism to a protein reactive species, it is possible that genetic differences in metabolism may play a role in the differential susceptibility of individuals to the development of contact hypersensitivity responses to these materials. 

McHale, J.F., et al., Vascular endothelial cell expression of ICAM-1 and VCAM-1 at the onset of eliciting contact hypersensitivity in mice evidence for a dominant role of TNF-a. J. Immunol, 162,1648-1655, 1999. 

Grabbe, S. and Schwarz, T., Immunoregulatory mechanisms involved in elicitation of allergic contact hypersensitivity. Immunol. Today, 19, 37, 1998. 

Kalergis, A.M., et al., Modulation of fatty acid oxidation alters contact hypersensitivity to urushiols Role of aliphatic chain B-oxidation in processing and activation of urushiols. Journal of Investigative Dermatology, 108, 57, 1997. 

Shomick, L.P., etal., Mice deficient in IL-lbeta manifest impaired contact hypersensitivity to trinitrochlorobenzene. J. Exp. Med., 183, 1427, 1996. 

Rennert, P.D., et al., Essential role of lymph nodes in contact hypersensitivity revealed in lymphotoxin-a-deficient mice. J. Exp. Med., 193, 1227, 2001. 

Gorbachev, A.V. and Fairchild, R.L., Induction and regulation of T-cell priming for contact hypersensitivity. Crit. Rev. Immunol., 21, 451, 2001. 

Direct adverse immune responses to the agent itself in the form of hypersensitivity responses (anaphylaxis and delayed contact hypersensitivity). 

Sensitization can be evaluated in the well-known delayed contact hypersensitivity assay or the mouse local lymph node assay. 

Ring S, Schafer SC, Mahnke K, Lehr HA, Enk AH CD4+ CD25+ regula- 41 tory T cells suppress contact hypersensitivity reactions by blocking influx of effector T cells into inflamed tissue. 

Contact Hypersensitivity and Animal Model of Tolerance to Haptens... 

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