BCL-2 over expression in radio resistant B-1 cells from (NZB/NZW) F1 female mice
ABCD PBi


BCL-2 over expression in radio resistant B-1 cells from (NZB/NZW) F1 female mice

  • Autor: R R N Brito
  • P Xander; Mario Mariano; Meeting of the Brazilian Society for Immunology (31. 2006 Búzios)
  • Assuntos: IMUNOLOGIA
  • É parte de: Abstracts São Paulo, SP: Brazilian Society for Immunology, 2006
  • Notas: Disponível em CD-ROM
  • Descrição: Introduction and Aims: B-1 cells have been related with the pathogenesis of Systemic Lupus Erythematosus (SLE) (Eur. J. Immunol. 16:450-6, 1986). (B/W)F1 hybrid female mice spontaneously develop autoimmunity (Adv. Immunol. 37:269-390, 1985). Since the number of these cells is increased in the pleural and peritoneal cavities of these animals (J. Exp. Med. 157:202-18, 1983), we investigated whether elimination of peritoneal and pleural B-1 cells by local irradiation could affect the onset of the disease. Methods and Results: Peritoneal cells were characterized by flow cytometry and purification of B-1 cells was performed with magnetic beads. Protein extracts were evaluated by Western blot analysis. Results show that survival of irradiated (16 months) mice was higher when compared with non-irradiated animals (8 months). Irradiation lead to considerable decrease of B-1 cell population in BALB/c, NZB, NZW and male (B/W)F1 but not in female (B/W)F1 animals. Female (B/W)F1 mice had higher amounts of these cells in the peritoneal cavity even nine months after irradiation. We than investigated whether the radio resistance of B-1 cells from female (B/W)F1 mice could be related with over expression of the anti-apoptotic protein Bcl-2. Conclusion: A possible relationship between the radio resistance of B-1 cells and evolution of murine SLE was not established. However, our data suggest that the over expressed Bcl-2 anti-apoptotic protein by these cells may play a primordial role in
    maintaining B-1 cells survival in peritoneal cavity after ionizing radiation.
  • Editor: São Paulo
  • Data de criação/publicação: 2006
  • Formato: res. CI.030.
  • Idioma: Inglês