Do costimulator pathways change in degenerative disk disease?


Akyol S., Tanriverdi T., Hanci M.

Neurosurgery Quarterly, cilt.24, sa.1, ss.75-80, 2014 (SCI-Expanded, Scopus) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 24 Sayı: 1
  • Basım Tarihi: 2014
  • Doi Numarası: 10.1097/wnq.0b013e318275de31
  • Dergi Adı: Neurosurgery Quarterly
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE
  • Sayfa Sayıları: ss.75-80
  • İstanbul Üniversitesi-Cerrahpaşa Adresli: Hayır

Özet

Immune activation plays an important role in the degenerative disk disease, and for the immune reactions to take place, antigen-presenting cells and T lymphocyte should interact with each other. This interaction is possible with some costimulator molecules and there are 2 major costimulator pathways: CD28-CD80 and CD40-CD40L. The aim of this study is to show how costimulators change in both degenerated disk tissues and the peripheral blood of the patients with degenerative disk disease. Thus, 26 patients with degenerated disk disease and 14 autopsy cases as controls were included. From both the groups, disk samples were collected during surgery and the autopsy processes, respectively. Peripheral blood samples were taken through intravenous lines during preoperative routine work-up and intracardiac puncture from the controls. Flow cytometric methods were used for the following molecules: CD80, CD40, CD40L, CD28, CD19, and CD4 (Th). Flow sitometrik method: CD40, CD40L, CD19, CD28, CD4 (Th), and CD80. For the cytokine levels, the Luminex method was used for IL-2, IL-4, IL-10, and TGF-β. This study showed that costimulator molecules are increased significantly in both degenerated disk samples and peripheral blood of the patients, and further studies are required to understand the pathophysiological mechanisms behind the degeneration processes and to provide appropriate treatment modalities targeting the inflammation. Copyright © 2013 by Lippincott Williams & Wilkins.