Cerebrospinal fluid concentrations of soluble CD27 in HTLV-I associated myelopathy and multiple sclerosis

Abstract

Objectives-Stimulation of T lymphocytes via the T cell receptor strongly enhances CD27 membrane expression and induces the release of a soluble 32 kDa form of CD27 (sCD27). CD27 is a member of the TNF receptor family, a group of molecules that have important roles in lymphocyte diVerentiation and survival. Raised concentrations of sCD27 have been reported in various immunopathological conditions and there is evidence that this molecule can serve as a marker of T cell activation in vivo. Concentrations of sCD27 in CSF were compared between patients with T cell mediated neurological disease and noninflammatory controls. Also, the relation of CSF-sCD27 concentrations with clinical disease activity was investigated in patients with multiple sclerosis. Methods-Four groups were studied: (1) eight patients with HTLV-1 associated myelopathy/ tropical spastic paraparisis (HAM)/TSP), (2) eight HTLV-I carriers, (3) 41 patients with multiple sclerosis, and (4) 43 patients with other neurological disease (OND). Concentrations of CSFsCD27 were determined by enzyme linked immunosorbent assay (ELISA). Results-Quantification of CSF-sCD27 diVerentiates patients with HAM/TSP from HTLV-I carriers (p<0.01) and from patients with OND (p<0.001). Moreover, the multiple sclerosis patient group was diVerent from the OND group (p<0.0001). In patients with multiple sclerosis, CSFsCD27 concentrations were higher in 24 patients with clinically active disease than in 17 with clinically stable disease. In addition, most of the patients with multiple sclerosis with high sCD27 concentrations showed an increase in EDSS, whereas none of the patients with low sCD27 had an EDSS increase. Conclusions-As a reliable marker of immunological disease activity in inflammatory white matter disease is still not available, it is proposed that quantification of CSF-sCD27 concentrations is a good candidate. Also, it may serve as a tool to stratify neurological diseases in inflammatory and non-inflammatory states. (J Neurol Neurosurg Psychiatry 1999;66:791-793)

Bone-marrow transplantation fails to halt intrathecal lymphocyte activation in multiple sclerosis

“…Baseline CSF-sCD27 levels in the 10 BMT patients (median 112, range 6–480) were significantly higher (p<0.01) than those of the OND control group (median 4.0, range 0.0–21 U/ml), in accordance with previous findings 13 14. No significant difference was found between the MS control group (median 54.5, range 20–280 U/ml) and the BMT patients that were selected for highly aggressive disease courses (p = 0.49) 9…”

“…All samples were obtained during the same time period as the CSF samples taken from the trial patients after informed consent. sCD27 concentrations in CSF were quantified with an enzyme-linked immunosorbent assay kit (CLB, Amsterdam, The Netherlands) 13. Presence of CSF oligoclonal bands and IgG indices were tested using standard methodology 16…”

Cerebrospinal Fluid Level of Soluble CD27 Is Associated with Disease Severity in Neuromyelitis Optica Spectrum Disorder

“…CSF sCD27 of patients with a clinically isolated syndrome is associated with MS diagnosis and a high relapse rate [16]. MS patients with more active disease have significantly higher levels of CSF sCD27 than subjects with quiescent disease, and patients with a higher EDSS score show an increased CSF sCD27 concentration [11, 12]. In addition, a significant correlation has been found between CSF sCD27 titer and IgG index in MS patients [17].…”

“…CD27 is expressed in about 80% of peripheral blood T lymphocytes as a transmembrane homodimer with subunits of 50–55 kDa [11, 12]. T cell activation via the T cell receptor/CD3 complex results in a strong enhancement of CD27 membrane expression [13, 14].…”

“…The concentration of CSF sCD27 is elevated in MS patients, higher in patients with clinically active disease than in those with clinically stable disease, and also related to neurological dysfunction [11, 12]. CD27 may also be involved in NMOSD pathogenesis.…”