Urocanic acid (UCA) is an epidermal chromophore that undergoes trans to cis isomerization after UVB irradiation. cis-UCA is a potent inhibitor of cutaneous acquired immunity. The aim of this study was to explore the genes, which are upregulated by cis-UCA in normal human epidermal keratinocytes (NHEK) and investigated its role in vitro using human T-lymphocyte cell line, Jurkat cells. DNA microarray analysis and real-time PCR investigation revealed that cis-UCA, not trans-UCA, increased the expression of a gene encoding a b-galactoside-binding lectin, galectin-7, LGALS7B. Immunohistochemical study demonstrated that galectin-7 was highly expressed in the epidermis in the patients with actinic keratosis. Galectin-7 administration upregulated apoptosis and inhibited the expression of interleukin-2 (IL2) and interferon-c (IFNG) mRNA in Jurkat cells. Taken together, galectin-7 may play important roles in downregulating the functions of T lymphocytes after UVB irradiation and can be developed into novel immunosuppressive therapies for inflammatory skin diseases.
BRAF-activating somatic mutations often exist in malignant melanoma. The underlying molecular mechanism of somatic BRAF mutation inductions remained to be clear. Activation-induced cytidine deaminase (AID), a member of a cytidine deaminase family, and APOBEC3B induce somatic mutations and recently have been indicated to be involved in the pathomechanism of several kinds of cancers. The aim of this study was to explore the expression level of AID and APOBEC3B in BRAF-mutation-containing malignant melanoma. Immunohistochemical study demonstrated that 9 of 10 malignant melanomas with high AID expression had BRAF V600E mutation.Eight of them developed multiorgan metastases or multiple lymph node metastases afterwards. Although the size of the patient panel was small, the results indicate that there might be an association between AID expression and BRAF mutation in melanoma.
Human body odour and earwax type are genetically dependent on a single-nucleotide polymorphism (SNP) located in the ABCC11 gene. So far, it still remains to be clear how SNP in the ABCC11 gene is associated with human malodour. In a recent issue of Experimental Dermatology, Baumann et al. propose one of the underlying molecular pathways. Although one of the amino acid conjugated of the odorants, Cys-Gly-3-methyl-3-sulfanylhexanol (3M3SH), was not taken up by the transporter ABCC11, glutathione conjugate of 3MSH (SG-3MSH) was transported by ABCC11. Moreover, SG-3MSH was processed to 3M3SH by c-glutamyl-transferase 1 (GGT1), which was abundantly expressed in apocrine sweat glands. These findings may pave a way for the pharmacogenetics of human body odour and the development of innovative deodorant products. Many people nowadays worry about their own body or axillary odour and use deodorants and antiperspirants (1). The annual sales of these commercial products amount to over $1.9 billion in the United States. In the United Kingdom, more than 90% of women use deodorants or antiperspirants on a daily basis, while 80% of men do so (1). Therefore, it is not just only scientifically but also psychosocially and economically important to elucidate the molecular mechanism that underlie human body odour.Recent findings using gene technology have provided us with better understandings of the mechanism of human body odour.The first key discovery came from the study on the determinant of human earwax type (2).Earwax (cerumen) is a secretory product of ceruminous apocrine glands. Human earwax is a Mendelian trait consisting of wet and dry types. The wet cerumen phenotype is completely dominant over the dry type. The dry type is seen frequently (80-95%) among East Asians, but uncommon (0-3%) in populations of European or African origin. Yoshiura et al. demonstrated that a single-nucleotide polymorphism (SNP) 538G?A in the ABCC11 gene, encoding an ATP-driven pump, is responsible for determination of earwax. The AA genotype corresponds to dry earwax, and GA and GG to wet type (2).Apocrine sweat contains proteins and non-odoriferous steroids. Odour molecules are secreted as non-odorous precursors, which are metabolized by bacteria on the skin surface. For example, amino acid conjugate, Cys-Gly-3-methyl-3-sulfanylhexanol (3M3SH) is secreted by apocrine glands and then broken down to 3M3SH by bacterial depeptidase (3).Many decades ago, it was proposed that wet earwax is accompanied by a strong axillary odour and dry earwax goes along with a missing axillary odour (4). In 2010, Martin et al. clearly explained this association between the character of earwax and axillary odour by performing genetic study (5,6). This showed that individuals who are homozygotic for a SNP 538G>A in the ABCC11 gene have less of the characteristics axillary odorants.The 538G>A SNP predominates in Asians who usually lack typical body odour (7).In a recent issue of the journal, Baumann et al. elegantly reveal how ABCC11 functionally plays a role in...
There are increasing cases of wheat dependent exercise-induced anaphylaxis (WDEIA) with transcutaneous or transmucosal sensitization. Hydrolyzed wheat included in a certain brand of soap was identified as a cause of sensitization. The useful clues to detect this disorder consist of the patient's past usage of a soap containing hydrolyzed wheat, the appearance of cutaneous or mucosal symptoms after the intake of wheat or washing with this soap, and a high level of specific IgE for wheat gluten. Because hydrolyzed wheat is used as an additive in a wide variety of cosmetics, we should pay careful attention to the ingredients of cosmetics when observing WDEIA.
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