Negative selection, epitope mimicry and autoimmunity

Rose, Noel R.

doi:10.1016/j.coi.2017.08.014

Cited by 50 publications

(45 citation statements)

References 41 publications

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“…The underlying mechanisms may include viral infection creating an inflammatory milieu which favors aberrant immune responses and promoting expansion of host antibodies or lymphocytes, which are cross-reactive both with viral antigen and self-antigen (i.e. "molecular mimicry") (Fairweather et al, 2005;Rose, 2017). In animal models of MS, auto-reactive lymphocytes have been identified which cross-react with both CoV epitopes and human myelin (Desforges et al, 2019), suggesting that molecular mimicry might be a potential mechanism by which CoV infection could potentiate development of autoimmune neuropsychiatric sequelae.…”

Section: Post-infectious Autoimmunitymentioning

confidence: 99%

Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms

Troyer

Kohn

Hong

2020

Brain, Behavior, and Immunity

861

779

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Section: Post-infectious Autoimmunitymentioning

confidence: 99%

Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms

Troyer

Kohn

Hong

2020

Brain, Behavior, and Immunity

861

779

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“…Guillain‐Barré syndrome (GBS) is a postinfectious immune‐mediated neuropathy that includes the symptoms of flaccid paralysis. Molecular mimicry between the outer core structures of Campylobacter jejuni and host nerve gangliosides is one apparent cause of GBS, and instigates a tissue‐damaging autoimmune response that determines disease presentation . However, the exact mechanisms that lead to induction of nerve fiber demyelination and axonal damage after antecedent C. jejuni infection remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Human leukocyte antigen‐DQB1 polymorphisms and haplotype patterns in Guillain‐Barré syndrome

Hayat

Jahan

Das

et al. 2019

Ann Clin Transl Neurol

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Objective The etiology of Guillain‐Barré syndrome (GBS) remains enigmatic, although genetic and environmental factors are speculated to be associated with this autoimmune condition. We investigated whether polymorphisms and the haplotype structures of the human leukocyte antigen (HLA)‐DQB1 gene relate to the autoimmune response to infection and affect the development of GBS. Methods HLA‐DQB1 polymorphic alleles (*0201, *030x, *0401, *050x, *060x) were determined for 151 Bangladeshi patients with GBS and 151 ethnically matched healthy controls using sequence‐specific polymerase chain reaction. Pairwise linkage disequilibrium (LD) and haplotype patterns were analyzed based on D ́statistics and the genotype package in R statistics, respectively. Association studies were conducted using Fisher's exact test and logistic regression analysis. The Bonferroni method was applied to correct for multiple comparisons, whereby the P‐value was multiplied with the number of comparisons and denoted as Pc (Pc, P corrected). Results No associations were observed between HLA‐DQB1 alleles and susceptibility to disease in the comparison between GBS patients and healthy subjects. Haplotype 9 (DQB1*0303‐*0601) tended to be less frequent among patients with GBS than healthy controls (P = 0.006, OR = 0.49, 95% CI = 0.30–0.82; Pc = 0.06). Haplotype 5 (DQB1*0501‐*0602) and the DQB1*0201 alleles were more frequent in the Campylobacter jejuni‐triggered axonal variant of GBS (P = 0.024, OR = 4.06, 95% CI = 1.25–13.18; Pc = 0.24) and demyelinating subtype (P = 0.027, OR = 2.68, 95% CI = 1.17–6.17; Pc = 0.35), though these associations were not significant after Bonferroni correction. Interpretation This study indicates that HLA‐DQB1 polymorphisms are not associated with susceptibility to GBS. In addition, these genetic markers did not influence the clinical features or serological subgroup in patients with C. jejuni‐triggered axonal variant of GBS.

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“…1 Molecular mimicry is highly common, as represented by cross-reactive T-cell and B-cell recognition, but wellestablished examples in human diseases are still relatively rare. 1 Demonstration that molecular mimicry is a causative mechanism of disease has been challenging for several reasons. First, identification of pathogenic autoantibodies or autoreactive T cells is mandatory to show a causative role of molecular mimicry.…”

Section: Introductionmentioning

confidence: 99%

Experimental approach in research of Guillain–Barré syndrome: A range of pathogeneses mediated by molecular mimicry

Koga

2018

Clinical & Exp Neuroim

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Molecular mimicry between microbial antigens and host tissue is a highly attractive explanation for the pathogenesis of many autoimmune diseases. Among them, Guillain–Barré syndrome (GBS) is an excellent model to show the causal pathogenesis of molecular mimicry, because the epidemiological association of GBS with several infections has been established. The present review describes recent findings regarding the causative role of molecular mimicry in GBS that arises after infection with several different bacteria and viruses, including Campylobacter jejuni, Mycoplasma pneumoniae, cytomegalovirus, Haemophilus influenzae, Epstein–Barr virus, hepatitis E virus and Zika virus. Although many issues must be resolved to fully understand GBS pathogenesis, molecular mimicry is highly likely to be involved in the development of C. jejuni‐associated GBS and probably of M. pneumoniae‐associated GBS. Candidate autoantibodies that are generated in cytomegalovirus‐ and H. influenzae‐associated GBS types can also provide clues to the causal role of molecular mimicry. For other diseases associated with antecedent infections, clarification of pathogeneses is premature and warrants further research on molecular mimicry, as well as other autoimmune‐triggering mechanisms.

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Negative selection, epitope mimicry and autoimmunity

Cited by 50 publications

References 41 publications

Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms

Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms

Human leukocyte antigen‐DQB1 polymorphisms and haplotype patterns in Guillain‐Barré syndrome

Experimental approach in research of Guillain–Barré syndrome: A range of pathogeneses mediated by molecular mimicry

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