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Fas (CD95) and bcl-2 expression in active skin lesions of Behcet's disease

Date

2005

Author

Baris, YS
Yildiz, L
Senturk, N
Kandemir, B

Metadata

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Abstract

Over-expression of bcl-2 in lymphocytes has an important role in some immunological and inflammatory diseases. Fas (CD95) is a cell surface molecule that mediates receptor-triggered apoptosis in various cells including autoreactive T cells. In this study we investigated bcl-2 and Fas (CD95) expression in dermal lymphocytes in active skin lesions of Behcet's disease (BD) and in skin biopsy samples with chronic, non-specific inflammations. Tissue sections of 29 skin lesions of Behcet's disease and of 10 chronic non-spesific inflammatory process cases from the archives of the Ondokuz Mayis University's Pathology Department were immunohistochemically stained for bcl-2 and Fas (CD95), and lymphocytes in the dermal infiltrate were evaluated for cytoplasmic staining. bcl-2 staining was observed in the skin lesions of 22 cases (75.8%) of Behcet's disease. bcl-2 staining was detected in two (20%) control skin biopsy samples with non-specific chronic inflammation. Fas (CD95) positivity was not detected in lymphocytes in Behcet's disease-related skin lesions. Fas (CD95) staining was observed in only three skin biopsy samples with non-specific chronic inflammation. bcl-2 and Fas (CD95) staining values in Behcet's and non-specific inflammation groups were significantly different (P < 0.01); differences in the bcl-2 staining values between Behcet's patients with mucocutaneous involvement only and mucocutaneous and other systemic involvements were not significant (P > 0.05). Expression of bcl-2 and loss of Fas (CD95) expression in dermal lymphocytes may play a role in the development of skin lesions and may account for the chronic course with periodic exacerbations in BD.

Source

Journal of the European Academy of Dermatology and Venereology

Volume

19

Issue

5

URI

https://doi.org/10.1111/j.1468-3083.2005.01250.x
https://hdl.handle.net/20.500.12712/20965

Collections

  • PubMed İndeksli Yayınlar Koleksiyonu [6144]
  • Scopus İndeksli Yayınlar Koleksiyonu [14046]
  • WoS İndeksli Yayınlar Koleksiyonu [12971]



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