Disease relevance of Uvbi1

• We have previously reported that UVB-induced immunosuppression of contact hypersensitivity was greatly enhanced in XPA mice [1].
• As UVB-induced immunosuppression has been implicated in the development of skin cancer, we investigated whether silymarin can modulate the effects of UVB radiation on the immune system [2].

High impact information on Uvbi1

• However, such exposure to UVA radiation has been observed unexpectedly to induce resistance to UVB-induced immunosuppression in mice, by a mechanism resulting in the inactivation of cis-urocanic acid (UCA), an epidermal immunosuppressive UV photoproduct [3].
• The phenotype of antigen-specific suppressor lymphocytes induced by painting oxazalone on the unirradiated skin of mice exposed once to UVB radiation was Lyt-1+2-, also a finding consistent with the hypothesis that the two forms of UVB-induced immunosuppression occur by means of the same mechanism [4].
• Prevention of UVB-induced immunosuppression in mice by the green tea polyphenol (-)-epigallocatechin-3-gallate may be associated with alterations in IL-10 and IL-12 production [5].
• Clinical testing shows that liposome-encapsulated T4 endonuclease V or photolyase stimulates repair of CPDs in the skin of human subjects, and prevents UVB-induced immunosuppression [6].
• TNF-alpha produces morphological changes in Langerhans cells indistinguishable from those induced by UVB exposure and antibodies against TNF-alpha have been demonstrated to inhibit UVB-induced immunosuppression in vivo [7].

Chemical compound and disease context of Uvbi1

• A high SPF sunscreen's effects on UVB-induced immunosuppression of DNCB contact hypersensitivity [8].

Biological context of Uvbi1

• In addition, in an in vivo mouse model, topical application of NAC (3 mumol cm-2) that has been shown to inhibit UVB-induced immunosuppression did not have any effect on UVB-induced apoptosis and did not reduce the formation or enhance the repair of UVB-induced cyclobutane pyrimidine dimers and (6-4) photoproducts [9].
• Topical treatment with EGCG on mouse skin also results in prevention of UVB-induced immunosuppression, and oxidative stress [10].
• N-acetylcysteine (NAC) has been shown to be an effective protector against UVB-induced immunosuppression and to modulate the expression of some oncogenes and tumor suppressor genes [9].
• These studies indicate that altered gene expression plays a pivotal role in UVB-induced immunosuppression [11].

Anatomical context of Uvbi1

• Cis-urocanic acid synergizes with histamine for increased PGE2 production by human keratinocytes: link to indomethacin-inhibitable UVB-induced immunosuppression [12].
• 3. Earliest-acting intermediates in the initiation of UVB-induced immunosuppression are the UVB absorbers (photoreceptors) of the skin, notably DNA resulting in immunoregulatory cytokine production, and trans-urocanic acid (UCA), which, upon isomerization to its cis isomer, signals downstream immunosuppressive events [13].

Associations of Uvbi1 with chemical compounds

• Surprisingly, the protective efficacy of NAC against UVB-induced immunosuppression was not affected by the BSO pretreatment [14].
• UVB-induced immunosuppression, a promoter of photocarcinogenesis, involves the formation of pyrimidine dimers and cis-urocanic acid (cis-UCA), but reactive oxygen species (ROS) also plays an important role [15].

Other interactions of Uvbi1

• OBJECTIVES: To clarify further the role of TNF-alpha in UVB-induced immunosuppression and in cis-UCA immunosuppression [7].
• In the present investigations, the effects of irradiation with UVA and UVB on the Fas(CD95)/FasL system have been studied because apoptosis mediated by the interaction between Fas and FasL has been suggested recently to be associated with UVB-induced immunosuppression in mouse skin [16].

References