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Published on: September 18, 2011
Compromised T-cell immunity in patients with spinal cord injury and its relationship with injury characteristics
Ozgur Kartal1, Bilge Yilmaz2, Mustafa Gülec3
1Department of Immunology and Allergic Diseases, Gülhane Faculty of Medicine and Gülhane Training and Research Hospital, University of Health Sciences, Ankara, Türkiye.
Objectives:
The aim of this study was to investigate in vivo and in vitro cellular immune responses in patients with chronic (spinal cord injury; SCI), determine the effects of autonomic dysfunction on cellular immune response, and determine the effect of completeness of the injury at different levels on cellular immune response.
Patients And Methods:
Forty-nine patients (42 males, 7 females; mean age: 35.5±13.4 years; range, 18 to 68 years) with chronic (time since injury >6 months) traumatic SCI were included in this cross sectional study between March 2013 and December 2013. Patients were allocated into two groups: Group 1, patients with an injury at T7 or below, and Group 2, patients with an injury at T6 or above. All patients in Group 2 had a history of autonomic dysreflexia and orthostatic hypotension. Intradermal skin tests were applied to the participants to reveal delayed T-cell responses. The percentages of cluster of differentiation (CD)3+ T cells and CD3+ T cells expressing CD69 and CD25 were analyzed by flow cytometry for the detection of activated T cells including all T-cell subsets.
Results:
When patients with complete injuries were compared, the CD45+ cell percentage was found to be significantly higher in patients in Group 2. Patients with an incomplete SCI had increased skin response to candida antigens compared to complete SCI patients. Incomplete SCI patients also had higher percentages of lymphocytes and CD3+CD25+ and CD3+CD69+ T cells compared to patients with complete SCI.
Conclusion:
T-cell activity is impaired in chronic SCI patients with higher levels of injury, and the completeness of injury and autonomic dysfunction gain prominence as compromising factors in T-cell immunity.
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