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Kronik lenfositik lösemide CD49d molekülü ve fibronektin adezyonunun incelenmesi

Başlık çevirisi mevcut değil.

  1. Tez No: 44498
  2. Yazar: EMEL EKŞİOĞLU (DEMİRALP)
  3. Danışmanlar: PROF.DR. TEVFİK AKOĞLU
  4. Tez Türü: Doktora
  5. Konular: Allerji ve İmmünoloji, Allergy and Immunology
  6. Anahtar Kelimeler: Belirtilmemiş.
  7. Yıl: 1995
  8. Dil: Türkçe
  9. Üniversite: Marmara Üniversitesi
  10. Enstitü: Sağlık Bilimleri Enstitüsü
  11. Ana Bilim Dalı: Belirtilmemiş.
  12. Bilim Dalı: Belirtilmemiş.
  13. Sayfa Sayısı: 89

Özet

Kronik lenfositik Löseminin başlıca özelliği olan periferik lenfositoz, lenfositler ile kemik iliği stromal elemanları ve stroma hücreleri arasında adezyon bozukluğu olduğunu düşündürmektedir. Son yıllarda tanımlanan çok sayıda adezyon molekülünden biri olan CD49d hem fibronektine, hem de en azından bir hücresel Uganda (VCAM-1) sahip çift etkili bir moleküldür. Bu çalışmada 62 KLL'li hasta ile, diğer hematolojik malignitelerde (n=40), sağlıklı kontrollerde (n=43) ve ayrıca göbek kordon kanı CD5(+) B hücrelerinde(n=34) CD49d ekspresyonu incelendi. CD49d ekspresyonu KLL de %50±29 iken bu oran diğer hematolojik malignitelerde %80±11, sağlıklı kontrollerde %85±3, göbek kordon kanı CD19(+) hücrelerinde %96±4 idi (p

Özet (Çeviri)

7. SUMMARY One of the characteristic feature of CLL is peripheral lymphocytosis which may suggest abnormal adhesion between extracellular matrix components, stroma cells of bone marrow and CLL lymphocytes. An adhesion molecule known as CD49d plays an important role in VCAM-1 mediated cellular and fibronectin mediated stromal adhesion in bone marrow. We investigated CD49d expression in 62 patients with CLL. We found that mean CD49d expression on CLL lymphocytes were significantly low, compared to that on normal peripheral lymphocytes (n=43) as well as on lymphocytes obtained from other hematological malignancies (n=40) and on CD5(+) B cells of umblical cord blood (n=34). Although mean CD49d expression was low, we have noticed that 24 % of the CLL patients were expressing normal but 76 % significantly diminished CD49d molecules on lymphocytes. When, patients' clinical stages were analysed according to CD49d status, it was found that RAI stage 0, 1 and II patients had low CD49d expression whereas RAI III and IV patients had normal CD49d. Furthermore other phenotypic analyses revealed presence of myeloid markers on lymphocytes in CD49d high and RAI stage III and IV cases. Taking together we suggest that CLL can be devided into two major subgroups: a)CD49dlow CD13(-) CD33(-) CDllalow TGF-Rlow sIgMlow b)CD49dh*h CD13(+) CD33(+) CDllahigh TGF-fih*h sIgMhigh. We have cultured normal, cord blood and CLL cells for 72 hours (samples were taken every 2 hours in the first 24 hours and later 48th and 72th hours) and analysed CD49d expression in the culture. We found that CD49d expression on lymphocytes of all three groups show fluctuations in the culture and CD49d expression of CLL lymphocytes reaches up to normal levels from time to time. Statistical methods were employed to analyse these fluctuations and revealed that all normal, cord blood and CLL cells show oscillations of equal period (approximately 30 hours). But 79the amplitudes of the oscillations in CLL cells were significantly higher. Adhesion of CLL cells to fibronectin was also investigated and compared with cord blood mononuclear cells and normal lymphocytes. We found that CLL cells with low CD49d expression had lower adhesion ratio whereas CD49d high CLL cells showed the normal ratio of adhesion. All these findings indicates that CD49d plays an important role in the peripheral lymphocytosis of CLL. 80

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