Journal of dermatological science · 2006
Nadifloxacin downmodulates antigen-presenting functions of epidermal Langerhans cells and keratinocytes.
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Murata Koji, Sugita Kazunari, Kobayashi Miwa, Kabashima Kenji, Tokura Yoshiki
Аннотация
BACKGROUND: Nadifloxacin is an anti-microbial quinolone derivative widely used for the treatment of acne as a topical agent. This drug has been suggested to have not only anti-bacterial but also anti-inflammatory actions, which may have a beneficial effect on some aspects of inflammatory acne.
OBJECTIVE: To further clarify its abilities to modulate skin immunity, we investigated whether nadifloxacin affects the hapten- and superantigen-presenting capacities of epidermal Langerhans cells (LC) and keratinocytes, respectively.
METHODS: Immune lymph node CD4+ T cells from trinitrophenyl-sensitized BALB/c mice were cocultured with LC-enriched epidermal cells (LC-EC) that were freshly isolated from syngeneic mice and derivatized with trinitrophenyl hapten in the presence or absence of nadifloxacin. Alternatively, LC-EC were preincubated with nadifloxacin (NDFX), modified with the hapten, and cultured with immune T cells. The effects of nadifloxacin on the surface molecule expression in LC and keratinocytes were also tested by flow cytometry and cellular ELISA.
RESULTS: LC-EC cultured with nadifloxacin at 10 microg/ml or more significantly suppressed the antigen-presenting function of LC for T cells. The ability of MHC class II+ keratinocytes to present a superantigen to T cells was suppressed by preincubation of keratinocytes with 30 microg/ml or more of nadifloxacin. These functional reductions in LC and keratinocytes reflected the decreased expression of MHC class II and/or costimulatory molecules.
CONCLUSION: Nadifloxacin downmodulates cutaneous immunity by interfering with the antigen-presenting ability of epidermal cells.
OBJECTIVE: To further clarify its abilities to modulate skin immunity, we investigated whether nadifloxacin affects the hapten- and superantigen-presenting capacities of epidermal Langerhans cells (LC) and keratinocytes, respectively.
METHODS: Immune lymph node CD4+ T cells from trinitrophenyl-sensitized BALB/c mice were cocultured with LC-enriched epidermal cells (LC-EC) that were freshly isolated from syngeneic mice and derivatized with trinitrophenyl hapten in the presence or absence of nadifloxacin. Alternatively, LC-EC were preincubated with nadifloxacin (NDFX), modified with the hapten, and cultured with immune T cells. The effects of nadifloxacin on the surface molecule expression in LC and keratinocytes were also tested by flow cytometry and cellular ELISA.
RESULTS: LC-EC cultured with nadifloxacin at 10 microg/ml or more significantly suppressed the antigen-presenting function of LC for T cells. The ability of MHC class II+ keratinocytes to present a superantigen to T cells was suppressed by preincubation of keratinocytes with 30 microg/ml or more of nadifloxacin. These functional reductions in LC and keratinocytes reflected the decreased expression of MHC class II and/or costimulatory molecules.
CONCLUSION: Nadifloxacin downmodulates cutaneous immunity by interfering with the antigen-presenting ability of epidermal cells.