The role of IL‐12 and TNF‐α in AIDP and AMAN

Deng, Hui; Yang, Xin; Jin, Taiyi; Wu, Jing; Hu, Lingzhen; Chang, Ming Shi; Sun, Xiguang; Adem, Abdu; Winblad, Bengt; Zhu, Jie

doi:10.1111/j.1468-1331.2008.02261.x

Cited by 26 publications

(17 citation statements)

References 22 publications

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“…Th1 and its cytokines are the pathogenic molecules in GBS as we reported previously [7, 8]. In the present study, we found that Th17 and Th22 cells and their cytokines may also contribute to the pathogenesis of GBS.…”

Section: Discussionsupporting

confidence: 86%

“…The pathogenesis of GBS remains still enigmatic, but it is largely accepted that both cellular and humoral immune responses are involved in the pathogenesis of GBS [5, 6]. AIDP and its animal model experimental autoimmune neuritis (EAN) have hitherto been classified to Th1 cells-mediated disorders [7–9]. Th1 cells, a subset of CD4 + T (T helper) cells, are dominant in the inflamed nerves at the acute phase of GBS [8], which could produce IFN- γ as a major pathogenic cytokine in GBS, because increased IFN- γ was seen in the serum of GBS patients at acute phase [10], and higher immunoreactivity for IFN- γ was showed in sural nerves biopsies of GBS patients [11].…”

Section: Introductionmentioning

confidence: 99%

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Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments

Jin

Zhang

et al. 2014

Mediators of Inflammation

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The Guillain-Barré syndrome (GBS) is considered a T helper 1 (Th1) cells-mediated acute inflammatory peripheral neuropathy. However, some changes in GBS could not be explained completely by Th1 cells pathogenic role. Recently, Th17 cells have been identified and can mediate tissue inflammation and autoimmune response. Therefore, a study on the role of Th17 and Th22 cells and their cytokines in GBS is necessary for exploring the pathogenesis of GBS. Here, we detected the frequency of Th1, Th17, and Th22 cells by using 4-color flow cytometry and we detected the plasma levels of IL-17 and IL-22 by ELISA in GBS patients, relapsing-remitting multiple sclerosis patients at the acute phase of relapse, viral encephalitis or meningitis patients and healthy controls. Our data showed that the frequency of circulating Th1, Th17, and Th22 cells was significantly increased in GBS patients. The plasma levels of IL-17 and IL-22 in GBS and relapsing-remitting multiple sclerosis at the acute phase of relapse were also markedly elevated. Enhanced circulating Th22 cells were correlated with GBS severity. Intravenous immunoglobulin therapy downregulated Th17, and Th22 cells and the plasma levels of IL-17 and IL-22 in GBS patients. Th17 and Th22 cells may be involved in the pathogenesis of GBS, and intravenous immunoglobulin mediates therapeutic effects by downregulating these cells and their cytokines.

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Section: Discussionsupporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments

Jin

Zhang

et al. 2014

Mediators of Inflammation

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“…4A,E). The inflammatory mediator TNF-a plays a key role in the pathological processes of Guillain-Barré syndrome and CIDP (Radhakrishnan et al, 2004;Deng et al, 2008;Yang et al, 2008). TNF-a also induces cell-specific damage to Schwann cells in vitro (Boyle et al, 2005) and thus contributes to the development of inflammatory neuropathy.…”

Section: Discussionmentioning

confidence: 99%

Peripheral nerve pericytes modify the blood–nerve barrier function and tight junctional molecules through the secretion of various soluble factors

Shimizu

Sano

Abe

et al. 2010

Journal Cellular Physiology

126

119

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The objectives of this study were to establish pure blood-nerve barrier (BNB) and blood-brain barrier (BBB)-derived pericyte cell lines of human origin and to investigate their unique properties as barrier-forming cells. Brain and peripheral nerve pericyte cell lines were established via transfection with retrovirus vectors incorporating human temperature-sensitive SV40 T antigen (tsA58) and telomerase. These cell lines expressed several pericyte markers such as α-smooth muscle actin, NG2, platelet-derived growth factor receptor β, whereas they did not express endothelial cell markers such as vWF and PECAM. In addition, the inulin clearance was significantly lowered in peripheral nerve microvascular endothelial cells (PnMECs) through the up-regulation of claudin-5 by soluble factors released from brain or peripheral nerve pericytes. In particular, bFGF secreted from peripheral nerve pericytes strengthened the barrier function of the BNB by increasing the expression of claudin-5. Peripheral nerve pericytes may regulate the barrier function of the BNB, because the BNB does not contain cells equivalent to astrocytes which regulate the BBB function. Furthermore, these cell lines expressed several neurotrophic factors such as NGF, BDNF, and GDNF. The secretion of these growth factors from peripheral nerve pericytes might facilitate axonal regeneration in peripheral neuropathy. Investigation of the characteristics of peripheral nerve pericytes may provide novel strategies for modifying BNB functions and promoting peripheral nerve regeneration.

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“…Such molecules include TNF-α, IL-1β, interleukin-12 (IL-12), interleukin-2 (IL-2), interleukin-6 (IL-6), neopterin (a by-product of guanosine triphosphate metabolism produced by macrophages in response to lymphocyte activation), osteopontin, ICAM-1, E-selectin, IFN-γ, interleukin-18 (IL-18), matrix metalloproteinase 9 (MMP-9), vascular cell adhesion molecule-1 (VCAM-1), interleukin-1 receptor antagonist (IL-1RA), interleukin-37 (IL-37) α6β4 integrin (laminin receptor for Schwann cells and myelin) and vascular endothelial growth factor (VEGF) [96,28,53,93,76,7,44,72,42,117,122]. More recently, elevated plasma levels of interleukin-17 (IL-17) and interleukin-22 (IL-22) have been described in patients with GBS, with reduced levels seen following treatment with intravenous immunoglobulin [73,42].…”

Section: Introductionmentioning

confidence: 99%

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

Ubogu

2015

Acta Neuropathol

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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.

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The role of IL‐12 and TNF‐α in AIDP and AMAN

Cited by 26 publications

References 22 publications

Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments

Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments

Peripheral nerve pericytes modify the blood–nerve barrier function and tight junctional molecules through the secretion of various soluble factors

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

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