Frequent IgG subclass and mannose binding lectin deficiency in patients with chronic fatigue syndrome

Guenther, Sabrina; Loebel, Madlen; Mooslechner, Agnes A.; Knops, Michael; Hanitsch, Leif G.; Grabowski, Patricia; Wittke, Kirsten; Meisel, Christian; Unterwalder, Nadine; Volk, Hans‐Dieter; Scheibenbogen, Carmen

doi:10.1016/j.humimm.2015.09.028

Cited by 34 publications

(47 citation statements)

References 39 publications

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“…It is tempting to speculate that patients, who can produce higher levels of TNFα and IFNα, have a more effective mucosal immunity and are therefore less prone to develop ME/CFS. This is in line with our previous observation, that a deficiency of the complement factor mannose binding lectin (MBL), which results in susceptibility to infections, is associated with ME/CFS (42).…”

Section: Discussionsupporting

confidence: 93%

Autoimmunity-Related Risk Variants in PTPN22 and CTLA4 Are Associated With ME/CFS With Infectious Onset

et al. 2020

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Section: Discussionsupporting

confidence: 93%

Autoimmunity-Related Risk Variants in PTPN22 and CTLA4 Are Associated With ME/CFS With Infectious Onset

et al. 2020

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“…Taken together, these results might indicate a role for B cells in CFS pathophysiology, as is supported from studies of cellular immunology: Brenu and co-workers reported a decrease in immature B cells and an increase in memory B cells among CFS patients [74], whereas Bradley and co-workers [75] and Mensah and co-workers [76] found subtle distortions in the proportion of B cell subsets. Alterations of immunoglobulin levels in CFS have also been reported [77], but was not identified in the present material, which is not surprising given the strong propensity of compensatory mechanisms to ensure normal immunoglobulin levels in circulation despite changes in B cell function [78]. …”

Section: Discussionmentioning

confidence: 48%

Whole blood gene expression in adolescent chronic fatigue syndrome: an exploratory cross-sectional study suggesting altered B cell differentiation and survival

et al. 2017

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BackgroundChronic fatigue syndrome (CFS) is a prevalent and disabling condition affecting adolescents. The pathophysiology is poorly understood, but immune alterations might be an important component. This study compared whole blood gene expression in adolescent CFS patients and healthy controls, and explored associations between gene expression and neuroendocrine markers, immune markers and clinical markers within the CFS group.MethodsCFS patients (12–18 years old) were recruited nation-wide to a single referral center as part of the NorCAPITAL project. A broad case definition of CFS was applied, requiring 3 months of unexplained, disabling chronic/relapsing fatigue of new onset, whereas no accompanying symptoms were necessary. Healthy controls having comparable distribution of gender and age were recruited from local schools. Whole blood samples were subjected to RNA sequencing. Immune markers were blood leukocyte counts, plasma cytokines, serum C-reactive protein and immunoglobulins. Neuroendocrine markers encompassed plasma and urine levels of catecholamines and cortisol, as well as heart rate variability indices. Clinical markers consisted of questionnaire scores for symptoms of post-exertional malaise, inflammation, fatigue, depression and trait anxiety, as well as activity recordings.ResultsA total of 29 CFS patients and 18 healthy controls were included. We identified 176 genes as differentially expressed in patients compared to controls, adjusting for age and gender factors. Gene set enrichment analyses suggested impairment of B cell differentiation and survival, as well as enhancement of innate antiviral responses and inflammation in the CFS group. A pattern of co-expression could be identified, and this pattern, as well as single gene transcripts, was significantly associated with indices of autonomic nervous activity, plasma cortisol, and blood monocyte and eosinophil counts. Also, an association with symptoms of post-exertional malaise was demonstrated.ConclusionAdolescent CFS is characterized by differential gene expression pattern in whole blood suggestive of impaired B cell differentiation and survival, and enhanced innate antiviral responses and inflammation. This expression pattern is associated with neuroendocrine markers of altered HPA axis and autonomic nervous activity, and with symptoms of post-exertional malaise. Trial registration Clinical Trials NCT01040429Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-017-1201-0) contains supplementary material, which is available to authorized users.

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“…Some studies report inconsistent data, too. For example an expansion of transitional and naïve B cells and reduced plasmablast levels was reported in one study [14], but could not be confirmed in two other studies [4, 12]. Immune cell phenotype and function analyses are, of course, hampered by variations in sampling and methodological differences between laboratories as most flow cytometric assays are not standardized.…”

Section: Discussionmentioning

confidence: 99%

The European ME/CFS Biomarker Landscape project: an initiative of the European network EUROMENE

et al. 2017

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Myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS) is a common and severe disease with a considerable social and economic impact. So far, the etiology is not known, and neither a diagnostic marker nor licensed treatments are available yet. The EUROMENE network of European researchers and clinicians aims to promote cooperation and advance research on ME/CFS. To improve diagnosis and facilitate the analysis of clinical trials surrogate markers are urgently needed. As a first step for developing such biomarkers for clinical use a database of active biomarker research in Europe was established called the ME/CFS EUROMENE Biomarker Landscape project and the results are presented in this review. Further we suggest strategies to improve biomarker development and encourage researchers to take these into consideration for designing and reporting biomarker studies.

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Frequent IgG subclass and mannose binding lectin deficiency in patients with chronic fatigue syndrome

Cited by 34 publications

References 39 publications

Autoimmunity-Related Risk Variants in PTPN22 and CTLA4 Are Associated With ME/CFS With Infectious Onset

Autoimmunity-Related Risk Variants in PTPN22 and CTLA4 Are Associated With ME/CFS With Infectious Onset

Whole blood gene expression in adolescent chronic fatigue syndrome: an exploratory cross-sectional study suggesting altered B cell differentiation and survival

The European ME/CFS Biomarker Landscape project: an initiative of the European network EUROMENE

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