Contact hypersensitivity response

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. 

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. 

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... 

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. 

Bestak R, Bametson RSC, Nearn MR, Halliday GM. Sunscreen protection of contact hypersensitivity responses from chronic solar-stimulated ultraviolet irradiation correlates with the absorption spectrum of sunscreen. J Invest Dermatol 1995 105 345-51. 

In addition to eliciting a contact hypersensitivity response, benzo[a]pyrene has been shown to suppress this response, to other sensitizers. The effects of dermally applied benzo[a]pyrene (alone or following dermal pretreatment with the prostaglandin synthetase inhibitor, indomethacin) on contact hypersensitivity (cell-mediated immunity), and production of antibodies to dinitrophenol (DNP) (humoral immunity) were studied in male BALB/c mice treated for 6 weeks to 6 months (Andrews et al. 1991a). A group of mice treated with acetone served as controls. Benzo[a]pyrene alone caused a significant reduction (p<0.01) in the contact hypersensitivity response to dinitrofluorobenzene (DNFB) as measured by increases in ear thickness when compared to the vehicle controls. However, indomethacin pretreatment prevented the benzo[a]pyrene-induced contact hypersensitivity response. Benzo[a]pyrene also reduced antibody titres to DNP in treated mice. This suppressive effect on humoral immune function was not restored by pretreatment with indomethacin. These findings led the authors to conclude that the mechanism of... 

Contact hypersensitivity response and skin swelling in mice were inhibited by topical application of tea tree oil, a-terpineol, or terpinen-4-ol however, ultraviolet B- or irritant-induced sweUiug was not suppressed. ... 

Gollnick, S.O., Musser, D.A., Oseroff, A.R., Vaughan, L.A., Owczarczak, B., and Henderson, B.W., lL-10 does not play a role in cutaneous Photofrin photodynamic therapy-induced suppression of the contact hypersensitivity response, Photochem. Photobiol, 74, 811, 2001. 

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. 

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. 

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. 

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

A second form of delayed-type hypersensitivity response is similar to that of contact dermatitis in that macrophages are the primary effector cells responsible for stimulating CD4+ T cells however, this response is not necessarily localized to the epidermis. A classical example of this type of response is demonstrated by the tuberculin diagnostic tests. To determine if an individual has been exposed to tuberculosis, a small amount of fluid from tubercle bacilli cultures is injected subcutaneously. The development of induration after 48 h at the site of injection is diagnostic of prior exposure. 

Topical drug preparations are applied for days or even weeks, cosmetics for a lifetime and skin contact is probably the most common form of exposure to industrial chemicals. Therefore, a knowledge of the cutaneous toxicity is important for an overall hazard assessment. Cutaneous toxicity or localised skin injury can be considered as a primary event, because the compound could be irritant or corrosive, or as a secondary immunologically mediated event causing a delayed hypersensitivity response. 

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