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Galectin‐7, induced by cis ‐urocanic acid and ultraviolet B irradiation, down‐modulates cytokine production by T lymphocytes
Author(s) -
Yamaguchi Takashi,
Hiromasa Kana,
KabashimaKubo Rieko,
Yoshioka Manabu,
Nakamura Motonobu
Publication year - 2013
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12268
Subject(s) - jurkat cells , microbiology and biotechnology , urocanic acid , cytokine , epidermis (zoology) , downregulation and upregulation , galectin , biology , chemistry , cancer research , immunology , t cell , immune system , gene , biochemistry , amino acid , anatomy , histidine
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 β ‐galactoside‐binding lectin, galectin‐7, LGALS 7B. 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‐ γ ( 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.