Abstract
ObjectiveTo characterize the CSF cytokine profile in chronic inflammatory demyelinating polyneuropathy (CIDP) patients with IgG4 anti‐neurofascin 155 (NF155) antibodies (NF155+ CIDP) or those lacking anti‐NF155 antibodies (NF155− CIDP).MethodsTwenty‐eight CSF cytokines/chemokines/growth factors were measured by multiplexed fluorescent immunoassay in 35 patients with NF155+ CIDP, 36 with NF155− CIDP, and 28 with non‐inflammatory neurological disease (NIND).ResultsCSF CXCL8/IL‐8, IL‐13, TNF‐α, CCL11/eotaxin, CCL2/MCP‐1, and IFN‐γ were significantly higher, while IL‐1β, IL‐1ra, and G‐CSF were lower, in NF155+ CIDP than in NIND. Compared with NF155− CIDP, CXCL8/IL‐8 and IL‐13 were significantly higher, and IL‐1β, IL‐1ra, and IL‐6 were lower, in NF155+ CIDP. CXCL8/IL‐8, IL‐13, CCL11/eotaxin, CXCL10/IP‐10, CCL3/MIP‐1α, CCL4/MIP‐1β, and TNF‐α levels were positively correlated with markedly elevated CSF protein, while IL‐13, CCL11/eotaxin, and IL‐17 levels were positively correlated with increased CSF cell counts. IL‐13, CXCL8/IL‐8, CCL4/MIP‐1β, CCL3/MIP‐1α, and CCL5/RANTES were decreased by combined immunotherapies in nine NF155+ CIDP patients examined longitudinally. By contrast, NF155− CIDP had significantly increased IFN‐γ compared with NIND, and exhibited positive correlations of IFN‐γ, CXCL10/IP‐10, and CXCL8/IL‐8 with CSF protein. Canonical discriminant analysis of cytokines/chemokines revealed that NF155+ and NF155− CIDP were separable, and that IL‐4, IL‐10, and IL‐13 were the three most significant discriminators.InterpretationIntrathecal upregulation of type 2 helper T (Th2) cell cytokines is characteristic of IgG4 NF155+ CIDP, while type 1 helper T cell cytokines are increased in CIDP regardless of the presence or absence of anti‐NF155 antibodies, suggesting that overproduction of Th2 cell cytokines is unique to NF155+ CIDP.
Highlights
Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated disease involving the peripheral nerves
neurofascin 155 (NF155)+ CIDP patients showed a higher frequency of distal acquired demyelinating symmetric neuropathy (DADS) than NF155À CIDP patients (P = 0.0013), more than half of NF155+ CIDP patients (57.1%) had typical CIDP
cerebrospinal fluid (CSF) protein amounts and cell counts were higher in NF155+ CIDP patients than in NF155À CIDP and non-inflammatory neurological disease (NIND) patients (Fig. 1A)
Summary
Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated disease involving the peripheral nerves. Both cell-mediated and humoral immunity are thought to play pathogenic roles in CIDP.[1]. The precise mechanisms of CIDP remain to be elucidated, mainly because CIDP encompasses etiologically heterogeneous conditions. Subsets of CIDP patients were reported to harbor a 2019 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.
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