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T. Ubuka - One of the best experts on this subject based on the ideXlab platform.

  • Identification ofS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-3-mercaptopyruvic Acid with a metabolic intermediate betweenS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-l-cysteine andS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-3-mercaptolactic Acid
    Amino Acids, 1997
    Co-Authors: M. Kinuta, H. Shimizu, N. Masuoka, J. Ohta, T. Ubuka
    Abstract:

    S -[2-Carboxy-1-(1 H -imidazol-4-yl)ethyl]-3-mercaptopyruvic Acid ( I ) was chemically synthesized in 15% yield by incubating a reaction mixture of trans -urocanic Acid and 3-fold excess of 3-mercaptopyruvic Acid at 45°C for 6 days. The synthesized compound was characterized by fast-atom-bombardment mass spectrometry and high-voltage paper electrophoresis. Compound I was identified with a product of an enzymatic reaction of S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl]- l -cysteine ( II ) with rat liver homogenate in a phosphate buffer, pH 7.4. Compound I was degraded to S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl]-3-mercaptolactic Acid ( III ), a compound previously found in human urine [Kinuta et al. (1994) Biochem J 297: 475–478], by incubation with rat liver homogenate. From these results, we suggest that compound I is a metabolic intermediate for the formation of compound III from compound II . The present pathway follows a formation of compound II from S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl] gluthathione [Kinuta et al. (1993) Biochim Biophys Acta 1157: 192–198], a proposed metabolite of l -histidine.

  • Preparation and characterization of S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]glutathione and its derivatives as proposed precursors of S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine, a compound found in human urine.
    Biochimica et biophysica acta, 1993
    Co-Authors: M. Kinuta, T. Ubuka, Satsuki Yamada, Keishi Yukihiro, Masaru Tomozawa
    Abstract:

    Formation of 3-[(carboxymethyl)thio]-3-(1H-imidazol-4-yl)propanoic Acid (I) and S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine (II), compounds found in human urine, has been demonstrated by enzymatic degradation of S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]glutathione (III). Compound (III) was chemically synthesized in 72% yield by incubating the reaction mixture of Trans-Urocanic Acid and 3-fold excess GSH at 65 degrees C for 1 wk, which was accompanied by formation of N-(S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteinyl)glycine (IV) in 15% yield. S-[2-Carboxy-1-(1H-imidazol-4-yl)ethyl]-N-gamma-glutamylcysteine (V) was produced by partial hydrolysis of compound (III) in HCl. The synthesized compounds were characterized mainly by fast-atom bombardment mass spectrometry and high-voltage paper electrophoresis as well as chemical degradation. Incubation of compound (III) with rat kidney homogenate in a Tris buffer (pH 8), formed compound (II) in 80% yield possibly via compound (IV). Yield of compound (II) was increased by adding glycylglycine to the reaction mixture. However, little degradation of compound (III) occurred in the use of rat liver, brain, heart or spleen homogenate as the enzyme source. Compound (II) was further metabolized to compound (I) by incubation with rat kidney homogenate in a phosphate buffer of pH 7.4. From these results, we suggest that the urinary compounds are products of enzymatic degradation of compound (III) and that GSH may participate in the metabolism of urocanic Acid, the first catabolite of L-histidine.

  • Isolation and characterization of 3-[(carboxymethyl)thio]-3-(1H-imidazol-4-yl)propanoic Acid from human urine and preparation of its proposed precursor, S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine.
    The Biochemical journal, 1991
    Co-Authors: M. Kinuta, N. Masuoka, J. Ohta, T Teraoka, T. Ubuka
    Abstract:

    3-[(Carboxymethyl)thio]-3-(1H-imidazol-4-yl)propanoic Acid (I) was isolated from healthy human urine by using ion-exchange column chromatography, and characterized by physicochemical analyses involving i.r., m.s. and n.m.r. spectrometries as well as chemical synthesis. The urinary content was 0.04-0.07 mumol/l. Compound (I) was synthesized by the addition of mercaptoacetic Acid to urocanic Acid. In order to establish the origin of the compound. S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine (II) and S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]glutathione (III) were produced by similar reactions of urocanic Acid with cysteine and GSH respectively. The yield of compound (II) was markedly increased by sunlight irradiation of the reaction mixture or by the use of cis-urocanic Acid rather than the trans isomer. Incubation of compound (II) with rat liver homogenate in a phosphate buffer, pH 7.40, formed a major and some minor products of enzymic degradation, one of which was identified with compound (I). Exposure of rats to the sunlight for 2 days resulted in increase of the epidermal content of Trans-Urocanic Acid from the normal value of 0.38 to 1.70 micrograms/mg wet wt. of skin, accompanied by formation de novo of the epidermal cis isomer. After sunlight irradiation, the content of the trans isomer decreased at a constant rate of 0.03 micrograms/mg wet wt. of skin per day, whereas the cis isomer was eliminated more quickly, having a phase of rapid decrease in the early period. From these results we suggest that compound (I) may participate in the metabolism of urocanic Acid and natural thiol compounds such as cysteine and GSH.

M. Kinuta - One of the best experts on this subject based on the ideXlab platform.

  • Identification ofS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-3-mercaptopyruvic Acid with a metabolic intermediate betweenS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-l-cysteine andS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-3-mercaptolactic Acid
    Amino Acids, 1997
    Co-Authors: M. Kinuta, H. Shimizu, N. Masuoka, J. Ohta, T. Ubuka
    Abstract:

    S -[2-Carboxy-1-(1 H -imidazol-4-yl)ethyl]-3-mercaptopyruvic Acid ( I ) was chemically synthesized in 15% yield by incubating a reaction mixture of trans -urocanic Acid and 3-fold excess of 3-mercaptopyruvic Acid at 45°C for 6 days. The synthesized compound was characterized by fast-atom-bombardment mass spectrometry and high-voltage paper electrophoresis. Compound I was identified with a product of an enzymatic reaction of S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl]- l -cysteine ( II ) with rat liver homogenate in a phosphate buffer, pH 7.4. Compound I was degraded to S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl]-3-mercaptolactic Acid ( III ), a compound previously found in human urine [Kinuta et al. (1994) Biochem J 297: 475–478], by incubation with rat liver homogenate. From these results, we suggest that compound I is a metabolic intermediate for the formation of compound III from compound II . The present pathway follows a formation of compound II from S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl] gluthathione [Kinuta et al. (1993) Biochim Biophys Acta 1157: 192–198], a proposed metabolite of l -histidine.

  • Preparation and characterization of S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]glutathione and its derivatives as proposed precursors of S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine, a compound found in human urine.
    Biochimica et biophysica acta, 1993
    Co-Authors: M. Kinuta, T. Ubuka, Satsuki Yamada, Keishi Yukihiro, Masaru Tomozawa
    Abstract:

    Formation of 3-[(carboxymethyl)thio]-3-(1H-imidazol-4-yl)propanoic Acid (I) and S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine (II), compounds found in human urine, has been demonstrated by enzymatic degradation of S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]glutathione (III). Compound (III) was chemically synthesized in 72% yield by incubating the reaction mixture of Trans-Urocanic Acid and 3-fold excess GSH at 65 degrees C for 1 wk, which was accompanied by formation of N-(S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteinyl)glycine (IV) in 15% yield. S-[2-Carboxy-1-(1H-imidazol-4-yl)ethyl]-N-gamma-glutamylcysteine (V) was produced by partial hydrolysis of compound (III) in HCl. The synthesized compounds were characterized mainly by fast-atom bombardment mass spectrometry and high-voltage paper electrophoresis as well as chemical degradation. Incubation of compound (III) with rat kidney homogenate in a Tris buffer (pH 8), formed compound (II) in 80% yield possibly via compound (IV). Yield of compound (II) was increased by adding glycylglycine to the reaction mixture. However, little degradation of compound (III) occurred in the use of rat liver, brain, heart or spleen homogenate as the enzyme source. Compound (II) was further metabolized to compound (I) by incubation with rat kidney homogenate in a phosphate buffer of pH 7.4. From these results, we suggest that the urinary compounds are products of enzymatic degradation of compound (III) and that GSH may participate in the metabolism of urocanic Acid, the first catabolite of L-histidine.

  • Isolation and characterization of 3-[(carboxymethyl)thio]-3-(1H-imidazol-4-yl)propanoic Acid from human urine and preparation of its proposed precursor, S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine.
    The Biochemical journal, 1991
    Co-Authors: M. Kinuta, N. Masuoka, J. Ohta, T Teraoka, T. Ubuka
    Abstract:

    3-[(Carboxymethyl)thio]-3-(1H-imidazol-4-yl)propanoic Acid (I) was isolated from healthy human urine by using ion-exchange column chromatography, and characterized by physicochemical analyses involving i.r., m.s. and n.m.r. spectrometries as well as chemical synthesis. The urinary content was 0.04-0.07 mumol/l. Compound (I) was synthesized by the addition of mercaptoacetic Acid to urocanic Acid. In order to establish the origin of the compound. S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine (II) and S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]glutathione (III) were produced by similar reactions of urocanic Acid with cysteine and GSH respectively. The yield of compound (II) was markedly increased by sunlight irradiation of the reaction mixture or by the use of cis-urocanic Acid rather than the trans isomer. Incubation of compound (II) with rat liver homogenate in a phosphate buffer, pH 7.40, formed a major and some minor products of enzymic degradation, one of which was identified with compound (I). Exposure of rats to the sunlight for 2 days resulted in increase of the epidermal content of Trans-Urocanic Acid from the normal value of 0.38 to 1.70 micrograms/mg wet wt. of skin, accompanied by formation de novo of the epidermal cis isomer. After sunlight irradiation, the content of the trans isomer decreased at a constant rate of 0.03 micrograms/mg wet wt. of skin per day, whereas the cis isomer was eliminated more quickly, having a phase of rapid decrease in the early period. From these results we suggest that compound (I) may participate in the metabolism of urocanic Acid and natural thiol compounds such as cysteine and GSH.

N. Masuoka - One of the best experts on this subject based on the ideXlab platform.

  • Identification ofS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-3-mercaptopyruvic Acid with a metabolic intermediate betweenS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-l-cysteine andS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-3-mercaptolactic Acid
    Amino Acids, 1997
    Co-Authors: M. Kinuta, H. Shimizu, N. Masuoka, J. Ohta, T. Ubuka
    Abstract:

    S -[2-Carboxy-1-(1 H -imidazol-4-yl)ethyl]-3-mercaptopyruvic Acid ( I ) was chemically synthesized in 15% yield by incubating a reaction mixture of trans -urocanic Acid and 3-fold excess of 3-mercaptopyruvic Acid at 45°C for 6 days. The synthesized compound was characterized by fast-atom-bombardment mass spectrometry and high-voltage paper electrophoresis. Compound I was identified with a product of an enzymatic reaction of S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl]- l -cysteine ( II ) with rat liver homogenate in a phosphate buffer, pH 7.4. Compound I was degraded to S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl]-3-mercaptolactic Acid ( III ), a compound previously found in human urine [Kinuta et al. (1994) Biochem J 297: 475–478], by incubation with rat liver homogenate. From these results, we suggest that compound I is a metabolic intermediate for the formation of compound III from compound II . The present pathway follows a formation of compound II from S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl] gluthathione [Kinuta et al. (1993) Biochim Biophys Acta 1157: 192–198], a proposed metabolite of l -histidine.

  • Isolation and characterization of 3-[(carboxymethyl)thio]-3-(1H-imidazol-4-yl)propanoic Acid from human urine and preparation of its proposed precursor, S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine.
    The Biochemical journal, 1991
    Co-Authors: M. Kinuta, N. Masuoka, J. Ohta, T Teraoka, T. Ubuka
    Abstract:

    3-[(Carboxymethyl)thio]-3-(1H-imidazol-4-yl)propanoic Acid (I) was isolated from healthy human urine by using ion-exchange column chromatography, and characterized by physicochemical analyses involving i.r., m.s. and n.m.r. spectrometries as well as chemical synthesis. The urinary content was 0.04-0.07 mumol/l. Compound (I) was synthesized by the addition of mercaptoacetic Acid to urocanic Acid. In order to establish the origin of the compound. S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine (II) and S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]glutathione (III) were produced by similar reactions of urocanic Acid with cysteine and GSH respectively. The yield of compound (II) was markedly increased by sunlight irradiation of the reaction mixture or by the use of cis-urocanic Acid rather than the trans isomer. Incubation of compound (II) with rat liver homogenate in a phosphate buffer, pH 7.40, formed a major and some minor products of enzymic degradation, one of which was identified with compound (I). Exposure of rats to the sunlight for 2 days resulted in increase of the epidermal content of Trans-Urocanic Acid from the normal value of 0.38 to 1.70 micrograms/mg wet wt. of skin, accompanied by formation de novo of the epidermal cis isomer. After sunlight irradiation, the content of the trans isomer decreased at a constant rate of 0.03 micrograms/mg wet wt. of skin per day, whereas the cis isomer was eliminated more quickly, having a phase of rapid decrease in the early period. From these results we suggest that compound (I) may participate in the metabolism of urocanic Acid and natural thiol compounds such as cysteine and GSH.

J. Ohta - One of the best experts on this subject based on the ideXlab platform.

  • Identification ofS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-3-mercaptopyruvic Acid with a metabolic intermediate betweenS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-l-cysteine andS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-3-mercaptolactic Acid
    Amino Acids, 1997
    Co-Authors: M. Kinuta, H. Shimizu, N. Masuoka, J. Ohta, T. Ubuka
    Abstract:

    S -[2-Carboxy-1-(1 H -imidazol-4-yl)ethyl]-3-mercaptopyruvic Acid ( I ) was chemically synthesized in 15% yield by incubating a reaction mixture of trans -urocanic Acid and 3-fold excess of 3-mercaptopyruvic Acid at 45°C for 6 days. The synthesized compound was characterized by fast-atom-bombardment mass spectrometry and high-voltage paper electrophoresis. Compound I was identified with a product of an enzymatic reaction of S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl]- l -cysteine ( II ) with rat liver homogenate in a phosphate buffer, pH 7.4. Compound I was degraded to S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl]-3-mercaptolactic Acid ( III ), a compound previously found in human urine [Kinuta et al. (1994) Biochem J 297: 475–478], by incubation with rat liver homogenate. From these results, we suggest that compound I is a metabolic intermediate for the formation of compound III from compound II . The present pathway follows a formation of compound II from S -[2-carboxy-1-(1 H -imidazol-4-yl)ethyl] gluthathione [Kinuta et al. (1993) Biochim Biophys Acta 1157: 192–198], a proposed metabolite of l -histidine.

  • Isolation and characterization of 3-[(carboxymethyl)thio]-3-(1H-imidazol-4-yl)propanoic Acid from human urine and preparation of its proposed precursor, S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine.
    The Biochemical journal, 1991
    Co-Authors: M. Kinuta, N. Masuoka, J. Ohta, T Teraoka, T. Ubuka
    Abstract:

    3-[(Carboxymethyl)thio]-3-(1H-imidazol-4-yl)propanoic Acid (I) was isolated from healthy human urine by using ion-exchange column chromatography, and characterized by physicochemical analyses involving i.r., m.s. and n.m.r. spectrometries as well as chemical synthesis. The urinary content was 0.04-0.07 mumol/l. Compound (I) was synthesized by the addition of mercaptoacetic Acid to urocanic Acid. In order to establish the origin of the compound. S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]cysteine (II) and S-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]glutathione (III) were produced by similar reactions of urocanic Acid with cysteine and GSH respectively. The yield of compound (II) was markedly increased by sunlight irradiation of the reaction mixture or by the use of cis-urocanic Acid rather than the trans isomer. Incubation of compound (II) with rat liver homogenate in a phosphate buffer, pH 7.40, formed a major and some minor products of enzymic degradation, one of which was identified with compound (I). Exposure of rats to the sunlight for 2 days resulted in increase of the epidermal content of Trans-Urocanic Acid from the normal value of 0.38 to 1.70 micrograms/mg wet wt. of skin, accompanied by formation de novo of the epidermal cis isomer. After sunlight irradiation, the content of the trans isomer decreased at a constant rate of 0.03 micrograms/mg wet wt. of skin per day, whereas the cis isomer was eliminated more quickly, having a phase of rapid decrease in the early period. From these results we suggest that compound (I) may participate in the metabolism of urocanic Acid and natural thiol compounds such as cysteine and GSH.

Mary Norval - One of the best experts on this subject based on the ideXlab platform.

  • cis-Urocanic Acid Initiates Gene Transcription in Primary Human Keratinocytes
    Journal of Immunology, 2008
    Co-Authors: Kazuyo Kaneko, Mary Norval, U Smetana-just, Mary Matsui, Antony R. Young, Susan John, Susan L. Walker
    Abstract:

    It is well established that solar UV radiation (UVR) suppresses cutaneous cell-mediated immunity in humans. trans -Urocanic Acid ( trans -UCA) is a major UVR-absorbing skin molecule that undergoes a photoisomerization to its cis -isomer following UVR exposure. Animal studies have demonstrated that cis -UCA plays a role in UVR-induced immune suppression, but the molecular mechanisms of action of cis -UCA are not fully understood. In this study, we examined changes in gene expression and synthesis of cytokines and PGE 2 following UCA treatment of primary human keratinocytes. A limited microarray analysis of keratinocytes from two donors indicated that ∼400 genes were induced by solar-simulated radiation (SSR), 16 of which were also up-regulated by cis -UCA. In contrast, trans -UCA had little or no effect on gene expression. The genes up-regulated by both cis -UCA and SSR were associated with apoptosis, cell growth arrest, cytokines, and oxidative stress. Further studies using primary keratinocytes from four new donors showed that PG-endoperoxide synthase-2 was dramatically induced by cis -UCA, resulting in an enhanced secretion of PGE 2 into the cell culture supernatant. cis -UCA also increased cytokine protein production such as that of TNF-α, IL-6, and IL-8 in a dose-dependent manner. SSR had the same effect as cis -UCA, but trans -UCA had no effect. In addition, activation of NF-κB and lipid peroxidation were induced by cis -UCA and SSR, but not trans -UCA, suggesting possible upstream events of the gene expression changes. The data suggest that the induction of immune suppression by cis -UCA may involve the initiation of gene transcription of immunomodulatory mediators in primary human keratinocytes.

  • Cis-urocanic Acid, a sunlight-induced immunosuppressive factor, activates immune suppression via the 5-HT2A receptor.
    Proceedings of the National Academy of Sciences of the United States of America, 2006
    Co-Authors: Jeffrey P. Walterscheid, Mary Norval, Dat X. Nghiem, Nasser Kazimi, Leta K. Nutt, David J. Mcconkey, Stephen E. Ullrich
    Abstract:

    Exposure to UV radiation induces skin cancer and suppresses the immune response. To induce immune suppression, the electromagnetic energy of UV radiation must be absorbed by an epidermal photoreceptor and converted into a biologically recognizable signal. Two photoreceptors have been recognized: DNA and Trans-Urocanic Acid (UCA). Trans-UCA is normally found in the outermost layer of skin and isomerizes to the cis isomer upon exposure to UV radiation. Although UCA was identified as a UV photoreceptor years ago, and many have documented its ability to induce immune suppression, its exact mode of action remains elusive. Particularly vexing has been the identity of the molecular pathway by which cis-UCA mediates immune suppression. Here we provide evidence that cis-UCA binds to the serotonin [5-hydroxytryptamine (5-HT)] receptor with relatively high affinity (Kd = 4.6 nM). Anti-cis-UCA antibody precipitates radiolabeled 5-HT, and the binding is inhibited by excess 5-HT and/or excess cis-UCA. Similarly, anti-5-HT antibody precipitates radiolabeled cis-UCA, and the binding is inhibited by excess 5-HT or excess cis-UCA. Calcium mobilization was activated when a mouse fibroblast line, stably transfected with the human 5-HT2A receptor, was treated with cis-UCA. Cis-UCA-induced calcium mobilization was blocked with a selective 5-HT2A receptor antagonist. UV- and cis-UCA-induced immune suppression was blocked by antiserotonin antibodies or by treating the mice with 5-HT2A receptor antagonists. Our findings identify cis-UCA as a serotonin receptor ligand and indicate that the immunosuppressive effects of cis-UCA and UV radiation are mediated by activation of the 5-HT2A receptor.

  • Photoimmunosuppression of contact hypersensitivity
    Expert Review of Dermatology, 2006
    Co-Authors: Mary Norval
    Abstract:

    Contact hypersensitivity is characterized by an antigen-specific T cell-mediated skin inflammation that occurs at the site of challenge with a hapten in individuals who have already generated an immune response to that hapten. A complex cascade follows ultraviolet irradiation of the skin and topical application of a hapten, ending in suppression of the contact hypersensitivity response. A variety of photoreceptors at the body surface initiate the process: these have been identified as DNA, Trans-Urocanic Acid and membrane components. Secondary steps follow, such as the production of a range of soluble immune mediators and changes in the number, phenotype and function of Langerhans cells, dendritic cells and macrophages. The final effector mechanisms include the expression of immunosuppressive cytokines, a change from a type 1 cytokine profile to type 2, the induction of hapten-specific T-regulatory cells and defective antigen presentation. The consequences of immunomodulation for skin cancer are considere...

  • The mechanisms and consequences of ultraviolet-induced immunosuppression
    Progress in Biophysics & Molecular Biology, 2006
    Co-Authors: Mary Norval
    Abstract:

    Exposure to ultraviolet radiation (UVR) can result in immune suppression to antigens encountered within a few days of the irradiation. The process leading to the down-regulation in immune responses is complex. It is initiated by several photoreceptors located in the skin surface, namely DNA, Trans-Urocanic Acid and membrane components. The absorption of UVR by these chromophores then leads to the release of a wide range of mediators that can affect antigen presenting cells locally or systemically. The final steps include the generation of antigen-specific T cells capable of regulating immunity. The consequences of the UV-induced changes in the skin immune system for the control of skin cancers, infectious diseases including vaccination, and autoimmune diseases are considered. Finally, the effects of active vitamin D, synthesised in the epidermis following UVR, are discussed in the context of the skin immune response.

  • Viability of the antigen determines whether DNA or urocanic Acid act as initiator molecules for UV-induced suppression of delayed-type hypersensitivity.
    Photochemistry and Photobiology, 2003
    Co-Authors: Angus M. Moodycliffe, Daniel B. Yarosh, Mary Norval, Margaret L. Kripke, Stephen E. Ullrich
    Abstract:

    Abstract UV radiation suppresses the immune response, and UV-induced immune suppression contributes to UV-induced photocarcinogenesis. For UV-induced immune suppression to occur, electromagnetic energy (i.e. UV radiation) must be converted to a biological signal. Two photoreceptors have been identified in the skin that serves this purpose, epidermal DNA and Trans-Urocanic Acid (UCA). Although compelling evidence exists to support a role for each pathway (UV-induced DNA damage or photoisomerization of UCA) in UV-induced immune suppression, it is not clear what determines which photoreceptor pathway is activated. To address this question, we injected UV-irradiated mice with a monoclonal antibody with specificity for cis-UCA or applied liposomes containing DNA repair enzymes to the skin of UV-irradiated mice. The effect that each had on UV-induced suppression of delayed-type hypersensitivity was measured. We asked whether the light source used (FS-40 sunlamps vs solar-simulated UV radiation) altered whicheve...