2007 Fiscal Year Final Research Report Summary
Claudin family in Langerhans cell in epidermis
| Project/Area Number |
18591243
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Yamaguchi University |
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Principal Investigator |
MORITA Kazumasa Yamaguchi University, Graduate School of Medicine, Dept. Dermatology, Associate Professor (40324652)
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| Co-Investigator(Kenkyū-buntansha) |
KANAZAWA Nobuo Wakayama Medical Univerrsiity, Graduate School of Medicine, Dept. Dermatology, Associate Professor (90343227)
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| Project Period (FY) |
2006 – 2007
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| Keywords | denderitic cell / Langerhans cell / keratinocyte / tight junction / claudin |
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| Research Abstract |
Claudins are integral membrane proteins at tight junctions (TJs), and play pivotal roles in formation and function of TJs. We investigated into claudin in dendritic cell in the skin. By RT-PCR and Western blotting, expression claudin-1 was confirmed in dendritic cell derived from bone marrow of normal mouse (BM-DC). In normal mouse epidermis, expression of claudin-1 was detected in Langerhans cell (intraepidermal dendritic cell) by immunofluorescence staining. In co-culture of normal human epidermal keratinocyte (NHEK) and BM-DC, concentration of claudin-1 was observed at cell-cell contact between NHEK and BMDC by immofluoresrence staining. In claudin-1 knockout newborn mouse, Langerhans cells were observed in epidermis, although the number seemed to be less than that in normal one. In claudin-1 knockout skin grafted onto nude mice, claudin-1-positive Langerhans cells migrated from nude mice observed in claudin- 1-negative epidermis. These finding showed that cell-cell interaction by claudin-1 is not necessary in terms of localization of Langerhans cell in epidermis. Finally, to know role of claudin-1 under stimulation by antigen, expression of claudin-1 was observed in BM-DC stimulated by LPS. By RT-PCR, expression of claudin-1 was decreased at Day 8 in LPS-stimulated BM-DC, compared to control. This finding suggested a mechanism which dendritic cell may migrate more easily by decrease of claudin-1 to recognize antigens such as LPS.
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