Th1 shift in CIDP versus Th2 shift in vasculitic neuropathy in CSF

Mei, Feng Jun; Ishizu, Takaaki; Murai, Hiroyuki; Osoegawa, Manabu; Minohara, Motozumi; Zhang, Kun Nan; Kira, Jun Ichi

doi:10.1016/j.jns.2004.10.001

Cited by 52 publications

(64 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have mostly shown a Th1 polarisation of the immune response in the blood and cerebrospinal fluid of CIDP patients 23 24. However, in one study, there was an increased proportion of IL4 secreting CD4 + T cells in the blood, suggesting a predominant Th2 response 25.…”

Section: Discussionmentioning

confidence: 80%

“…IL17-secreting T cells (Th17) are a subset of CD4 + T cells that have been recently recognised as highly pro-inflammatory and responsible for severe autoimmune reactions 28. Mei et al 23 reported an increase in the concentration of IL17, along with IL6 and IL8, in the cerebrospinal fluid of untreated CIDP patients compared with other neurological diseases. Recent studies have suggested that IL17, rather than IFNγ, plays a crucial role in the inflammatory responses in multiple sclerosis 29.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Humoral and cellular immune responses to myelin protein peptides in chronic inflammatory demyelinating polyradiculoneuropathy

Sanvito

Makowska

Mahdi-Rogers

et al. 2009

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

Antibodies to non-conformational antigenic epitopes of myelin proteins rarely occur in CIDP. None of the myelin protein peptides elicited IFN gamma responses, but P2 elicited IL10 responses significantly more often in CIDP patients than in controls. This reactivity may be part of an antigen-specific Th2 type pathogenetic or regulatory mechanism or represent a transitory epiphenomenon due to nerve damage. In our study, P2 was the protein antigen most likely to be involved in the aberrant immune responses in CIDP.

show abstract

Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Humoral and cellular immune responses to myelin protein peptides in chronic inflammatory demyelinating polyradiculoneuropathy

Sanvito

Makowska

Mahdi-Rogers

et al. 2009

Journal of Neurology, Neurosurgery & Psychiatry

View full text Add to dashboard Cite

show abstract

“…growth arrest specific 6, MMP-2, high cathepsin B with low cystatin C levels have been described. Increased levels of CSF CCL2, CCL7, CCL27, CXCL9, CXCL10, CXCL12, ICAM-1, VCAM1 and VEGF have been described in CIDP as seen with AIDP [84,117,118,94]. Elevated levels of CCL3, CCL19 (correlated with the CSF: plasma albumin ratio), stem cell factor (SCF) and hepatocyte growth factor (HGF) compared to GBS and other non-inflammatory controls have also been described [106].…”

Section: Introductionmentioning

confidence: 99%

“…Marked upregulation of Th1 cytokines, IL-17, and downregulation of Th2 cytokines, together with infiltration of IFN-γ-producing CD4+ T cells in the cerebrospinal fluid were proposed as useful diagnostic markers for CIDP [84]. In addition to higher in vitro mononuclear production of IL-10, IL-17 and IFN-γ in CIDP patients, elevated expression of pSTAT1, T-bet, and pSTAT3 has been proposed as markers of disease activity [75].…”

Section: Introductionmentioning

confidence: 99%

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Ubogu

2015

Acta Neuropathol

View full text Add to dashboard Cite

Inflammatory neuropathies encompass groups of heterogeneous disorders characterized by pathogenic immune-mediated hematogenous leukocyte infiltration of peripheral nerves, nerve roots or both, with resultant demyelination or axonal degeneration or both. Inflammatory neuropathies may be divided into three major disease categories: Guillain-Barré syndrome (particularly the acute inflammatory demyelinating polyradiculoneuropathy variant), Chronic inflammatory demyelinating polyradiculoneuropathy and nonsystemic vasculitic neuropathy (or peripheral nerve vasculitis). Despite major advances in molecular biology, pathology and genetics, the pathogenesis of these disorders remains elusive. There is insufficient knowledge on the mechanisms of hematogenous leukocyte trafficking into the peripheral nervous system to guide the development of specific molecular therapies for immune-mediated inflammatory neuropathies compared to disorders such as psoriasis, inflammatory bowel disease, rheumatoid arthritis or multiple sclerosis. The recent isolation and characterization of human endoneurial endothelial cells that form the blood-nerve barrier provides an opportunity to elucidate leukocyte-endothelial cell interactions critical to the pathogenesis of inflammatory neuropathies at the interface between the systemic circulation and peripheral nerve endoneurium. This review discusses our current knowledge of the classic pathological features of inflammatory neuropathies, attempts at molecular classification and genetic determinants, the utilization of in vitro and in vivo animal models to determine pathogenic mechanisms at the interface between the systemic circulation and the peripheral nervous system relevant to these disorders and prospects for future potential molecular pathology biomarkers and targets for specific therapeutic intervention.

show abstract

“…Cytokines, mainly Th1, are up-regulated in the blood [22] and cerebrospinal fluid of patients [23] and sural nerve biopsy shows infiltration of T cells and macrophages associated with endoneurial expression of chemokines and their receptors (Figure 1) [24]. Nevertheless more research is needed to establish the polarity and target of the T-cell response and whether other cell populations, like other leukocyte subtypes or the Schwann cell itself [25], are relevant to the pathogenesis.…”

Section: Pathogenesis Of Cidpmentioning

confidence: 99%

Chronic inflammatory demyelinating polyradiculoneuropathy: A role for haematopoietic stem cell transplantation?

2008

View full text Add to dashboard Cite

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a clinical syndrome of a chronic progressive or relapsing and remitting, symmetrical, sensory and motor radiculoneuropathy. The immune reaction in CIDP is characterised by selective inflammation of peripheral nerves and is probably due to the interaction of cellular and humoral responses. Only three treatments for CIDP have demonstrated benefit in randomised studies, corticosteroids, plasma exchange and intravenous immunoglobulin. 25% of patients fail to respond or do not respond adequately to these treatments. Experimental data in animal models have shown that several autoimmune disorders, either congenital or acquired, can be transferred and/or treated by the transplantation of bone marrow stem cells. Haematopoietic stem cell transplantation (HSCT) has been performed with varying success in over 700 patients with autoimmune disorders throughout Europe. The experience in CIDP is very limited. This article will review current understanding of CIDP and experience of the use of HSCT in refractory CIDP.

show abstract

Th1 shift in CIDP versus Th2 shift in vasculitic neuropathy in CSF

Cited by 52 publications

References 47 publications

Humoral and cellular immune responses to myelin protein peptides in chronic inflammatory demyelinating polyradiculoneuropathy

Humoral and cellular immune responses to myelin protein peptides in chronic inflammatory demyelinating polyradiculoneuropathy

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Chronic inflammatory demyelinating polyradiculoneuropathy: A role for haematopoietic stem cell transplantation?

Contact Info

Product

Resources

About