Fc receptor like 3 in Chinese patients of Han nationality with Guillain–Barré syndrome

Sang, Daoqian; Chen, Qiming; Liu, Xiaolin; Qu, Hongdang; Dao-xiang, Wei; Yin, Liang; Zhang, Lina

doi:10.1016/j.jneuroim.2012.03.006

Cited by 16 publications

(8 citation statements)

References 29 publications

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“…Yes (Sang et al, 2012) Not studied in CIDP Glucocorticoid receptor NRC31 5q31.3 Related to clinical course (Dekker et al, 2009) Not studied in CIDP G1M marker IGHG1 14q32.33 Yes (Feeney et al, 1989) No (Pandey et al, 2005) No (Feeney et al, 1989) G2M marker IGHG2 14q32.33 Yes (Feeney et al, 1989) No (Pandey et al, 2005) No (Feeney et al, 1989) G3M marker IGHG3 14q32.33 Yes (Feeney et al, 1989) No (Pandey et al, 2005) No (Feeney et al, 1989) Interleukin 10 IL 10 1q31 Linked to disease susceptibility (Myhr et al, 2003) Not studied in CIDP 19q13.4 No (Blum et al, 2013a) No studied in CIDP KM marker IGKC 2p12 Linked to antibody production (Pandey et al, 2005) Not studied in CIDP MBL MBL2 10q11.2 Linked to severity of GBS (Geleijins et al, 2006) Not studied in CIDP MMP9 MMP9 20q11.2 No effect on susceptibility, but link with severity (Geleijns et al, 2007) Not studied in CIDP T cell specific adaptor protein…”

Section: Fcgr3b 1q23mentioning

confidence: 99%

Genetics of Guillain‐Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): current knowledge and future directions

Blum

McCombe

2014

J Peripheral Nervous Sys

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Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are thought to be autoimmune diseases. There have been many attempts to find a human leukocyte antigen (HLA) association with GBS and CIDP with little success. There have been studies of other plausible genes in GBS and CIDP and the role of these genes in GBS and CIDP and the data from these genetic studies is reviewed. Some of the genes that have been studied are immune related and some others have nervous system effects. The studies are limited by small numbers. Some of the genes show association with disease severity rather than disease susceptibility. The need for more detailed molecular studies of the role of HLA molecules and the need for modern genetic approaches to GBS and CIDP are explained.

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Section: Fcgr3b 1q23mentioning

confidence: 99%

Genetics of Guillain‐Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): current knowledge and future directions

Blum

McCombe

2014

J Peripheral Nervous Sys

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“…33,34 Increased responsiveness to pathogen-associated molecules could explain the increased recurrence rate of GBS. Here, we demonstrate that former GBS patients exhibited increased DC responsiveness to C. jejuni LOS with respect to CD38 and CD40 expression.…”

Section: Discussionmentioning

confidence: 99%

“…These may include SNPs affecting expression and/or function of genes not directly linked to the TLR pathway, for example, the complement system, or inhibitory receptors expressed on B cells. 33,34 Increased responsiveness to pathogen-associated molecules could explain the increased recurrence rate of GBS. 9,10 Future studies should identify whether DCs from (former) GBS patients also exhibit increased responsiveness through other pattern recognition receptors, given that type I IFN production and CD38 upregulation are also known to occur in response to other TLR ligands, 35 particularly from viruses.…”

Section: Discussionmentioning

confidence: 99%

Innate Immunity to Campylobacter jejuni in Guillain‐Barré Syndrome

Huizinga

Berg

Rijs

et al. 2015

Annals of Neurology

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“…Fc γ RIIa, Fc γ RIIb, Fc γ RIIIa, and Fc γ RIIIb were found to be associated with the severity of GBS [ 22 , 23 ]. The frequencies of expression of FcRL3-3-169C, FcRL3-6 intron 3A, and FcRL3-8 exon 15G alleles were significantly higher in GBS patients compared with HCs [ 24 ].…”

Section: Biomarkers Of Gbs ( Table 1 )mentioning

confidence: 99%

Biomarkers of Guillain‐Barré Syndrome: Some Recent Progress, More Still to Be Explored

Wang

Sun

Zhu

et al. 2015

Mediators of Inflammation

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Guillain-Barré syndrome (GBS), the axonal subtype of which is mainly triggered by C. jejuni with ganglioside-mimicking lipooligosaccharides (LOS), is an immune-mediated disorder in the peripheral nervous system (PNS) accompanied by the disruption of the blood-nerve barrier (BNB) and the blood-cerebrospinal fluid barrier (B-CSF-B). Biomarkers of GBS have been extensively explored and some of them are proved to assist in the clinical diagnosis and in monitoring disease progression as well as in assessing the efficacy of immunotherapy. Herein, we systemically review the literature on biomarkers of GBS, including infection-/immune-/BNB, B-CSF-B, and PNS damage-associated biomarkers, aiming at providing an overview of GBS biomarkers and guiding further investigations. Furthermore, we point out further directions for studies on GBS biomarkers.

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Fc receptor like 3 in Chinese patients of Han nationality with Guillain–Barré syndrome

Cited by 16 publications

References 29 publications

Genetics of Guillain‐Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): current knowledge and future directions

Genetics of Guillain‐Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): current knowledge and future directions

Innate Immunity to Campylobacter jejuni in Guillain‐Barré Syndrome

Biomarkers of Guillain‐Barré Syndrome: Some Recent Progress, More Still to Be Explored

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