The association of the activation-inducible tumor necrosis factor receptor and ligand with lumbar disc herniation.
OBJECTIVE
Herniated nucleus pulposus fragments are recognized by the immune system as a foreign-body, which results in an autoimmune reaction. Human activation-inducible tumor necrosis factor receptor (AITR) and its ligand, AITRL, are important costimulatory molecules in the pathogenesis of autoimmune diseases. Despite the importance of these costimulatory molecules in autoimmune disease, their role in the autoimmune reaction to herniated disc fragments has yet to be explored. The purpose of the present study is to investigate whether the overexpression of AITR and AITRL might be associated with lumbar disc herniation.


METHODS
The study population consisted of 20 symptomatic lumbar disc herniation patients. Ten macroscopically normal control discs were obtained from patients with spinal fractures managed with anterior procedures that involved a discectomy. Peripheral blood samples from both the study patients and controls were collected. The expression levels of AITR and AITRL were investigated by flow cytometric analysis, confocal laser scanning microscopy, immunohistochemistry and by reverse transcriptase-polymerase chain reaction (RT-PCR). The soluble AITR and AITRL serum levels were measured by an enzyme-linked immunosorbent assay.


RESULTS
Flow cytometric analysis revealed significantly higher levels of both AITR and AITRL in the lumbar disc herniation patients than in the controls. The AITRL expression levels were also increased in patients with lumbar disc herniation, shown by using confocal laser scanning microscopy, immunohisto-chemistry, and RT-PCR. Finally, soluble AITR and AITRL were elevated in the patients with lumbar disc herniations.


CONCLUSIONS
The AITR and AITRL are increased in both the herniated disc tissue and the peripheral blood of patients with lumbar disc herniation.
Park
Moon-Soo
MS
Department of Orthopaedic Surgery, Hangang Sacred Heart Hospital, Hallym University College of Medicine, 94-200 Yeongdeungpo-dong, Yeong deungpo-gu, Seoul 150-719, Korea. amhangpark@yahoo.co.kr
Lee
Hwan-Mo
HM
Hahn
Soo-Bong
SB
Moon
Seong-Hwan
SH
Kim
Yung-Tae
YT
Lee
Choon-Sung
CS
Jung
Hyo-Won
HW
Kwon
Byoung-Se
BS
Riew
K Daniel
KD
D000328:Adult; D005260:Female; D005434:Flow Cytometry; D053450:Glucocorticoid-Induced TNFR-Related Protein; D006801:Humans; D007150:Immunohistochemistry; D007378:Interleukins / Q000097:blood; D007405:Intervertebral Disc Displacement / Q000276:immunology*; D008159:Lumbar Vertebrae; D008297:Male; D018613:Microscopy, Confocal; D008875:Middle Aged; D017475:Receptors, Nerve Growth Factor / Q000097:blood*; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D048069:Tumor Necrosis Factors / Q000097:blood*
D053450:Glucocorticoid-Induced TNFR-Related Protein; D007378:Interleukins; D017475:Receptors, Nerve Growth Factor; D018124:Receptors, Tumor Necrosis Factor; C491405:TNFRSF18 protein, human; C478967:TNFSF18 protein, human; D014409:Tumor Necrosis Factor-alpha; D048069:Tumor Necrosis Factors