Cytokine mapping in cerebrospinal fluid and blood in multiple sclerosis patients without oligoclonal bands

Abstract

OCB- MS patients do not seem to constitute a separate entity concerning inflammatory parameters measured as cytokine concentrations in CSF and blood.

Lack of association of the CD14/C −159T polymorphism with susceptibility and progression parameters in Turkish multiple sclerosis patients

“…Consequently elevated levels of sCD14 may suggest only a transitory macrophage activation limited to attacks. The lack of consistent difference of sCD14 levels between oligoclonal band positive and negative patients are in line with our results that sCD14 does not appear as a reliable inflammatory marker (Vrethem et al, 2011). Moreover Walter et al, reported no significant increase in either systemic or intrathecal release of sCD14 in MS patients, as compared to controls, regardless of the presence or absence of active disease (Walter et al, 2006).…”

Relation of intrathecal oligoclonal band production to inflammatory mediator and immunotherapy response in 208 children with OMS

“…In adult patients with multiple sclerosis, no cytokine differences were found based on presence or absence of OCB (Maimone et al, 1991). In another group of adults with multiple sclerosis, the concentrations of 13 cytokines were similar in OCB(+) and OCB(−) patients (Vrethem et al, 2012). The authors concluded that OCB(−) patients did not seem to constitute a separate entity concerning those inflammatory parameters, which they interpreted as supporting a mainly T-cell-driven mechanism Fig.…”

“…Abbreviations: CSF, cerebrospinal fluid; OCB, oligoclonal bands; ns, not statistically significant. (Vrethem et al, 2012), but they queried as to whether results for BAFF or CXCL13 might be different. In untreated optic neuritis, six cytokines did not discriminate between OCB(+) and OCB(−) patients (Kivisäkk et al, 1998).…”

“…Combinatorial assay panels utilizing multiple markers have aided mapping the patterns of inflammatory mediators (Edwards et al, 2013), including those that foster the survival of B cells and plasma cells in niches within the CNS (Pollok et al, 2017). While OCB production and chemokine/cytokine production has been compared in adults with multiple sclerosis (Vrethem et al, 2012), few other neuroinflammatory disorders have been interrogated in the same way, especially in children, and require elucidation.…”

Neuroinflammation in Neurological Dysfunction and Degeneration

“…Amyotrophic lateral sclerosis Serum: IL-6, IL-13, IL-17, TNF-α, MCP-1, CRP CSF: IFNγ Tissue: Translocator protein upregulation [20][21][22][23][24] [25] [26] Alzheimer's disease Serum: IL-6, IL-1β, TNF-α, CRP, TGF-β, IL-12, IL-18 CSF: TGF-β Tissue: Translocator protein upregulation [27,28] [27] [17] Huntington's disease Serum: IL-6, IL-8, IL-13, TNF-α CSF: IL-6, IL-8 Tissue: Translocator protein upregulation [29] [30] [31] Multiple sclerosis Serum: TNF-α, IFNγ, IL-1β, IL-6, IL-10, CXCL8, TGF-β CSF: TNF-α, IL-1β Tissue: Translocator protein upregulation [32,33] [34] [16] Parkinson's disease Serum: MCP-1, RANTES, MIP-1α, IL-8, IFNγ, IL-1β, TNF-α CSF: IL-1β, IL-6 Tissue: Translocator protein upregulation [35] [36] [18] II. NEURODEGENERATIVE DISORDERS…”