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Previous Names: "high-mobility group nonhistone chromosomal protein 1", "high-mobility group box 1". Omim: GenBank: D Cytogenetic location: 13q A ruler that provides location information. GRCh37 assembly. The blue boxes on this track indicate regions for which coordinates have been observed in PDB. This track represents the gene-structure on the genome. This track shows various repeat regions that have been annotated along the genome. Studies have suggested that immune response abnormalities in autoimmune diseases may result from the genetic and environmental factors. High mobility group box 1 HMGB1 is a group of non-histone nuclear protein by being actively secreted from activated immune cells or passively released from injured or dying cells and becomes a proinflammatory mediator via binding to various receptors such as RAGE, TLR-2, TLR-4, and TLR-9 on the surface of responding cells.

Therefore, whether HMGB1 as a proinflammatory mediator is associated with autoimmune diseases is still controversial. Relevant articles and studies up to October 1 were searched via the following electronic databases: PubMed, Medline, and Web of science databases. We recruited data only from the full-published paper and meeting or conference abstracts were excluded. Our search was limited to English language publications. In this meta-analysis , ethical approval was not necessary as all the data were based on the previous published studies. If the same study was reported in more than 1 publication, we considered largest sample size or the most recent publication were included, but only 1 was included.

Relevant articles and studies were excluded if any of following criteria were met: conference abstracts, editorials, reviews, meta-analyses, consensus statements, guidelines, case-only reports, and case report; studies were not performed in humans; studies with partially overlapping patient populations; and study with incomplete data. Two authors BZ and QZ conducted independently extracted the data and quality assessment. In most studies, the mean and deviation were obtained, but in several studies only the median and quartiles were reported.

Therefore, when the original data were median and quartiles, we transformed and calculated the data to gain the appropriate values according to the method recommended by Hozo et al. If original important data were unavailable in some articles, we contacted corresponding author by E-mails to obtain further details. The methodologic quality of the studies was evaluated using Newcastle—Ottawa quality assessment scale NOS. Stata The heterogeneity was evaluated by Cochrane Q statistic. Otherwise, the random effect model was selected.

Sensitivity analyze was used to evaluate the impact of single studies on overall outcomes. Publication bias was visually estimated by a funnel plot, Begg methods, and Egger linear regression test. To detect the sources of heterogeneity, further subgroup analysis was performed according to disease state, disease type, and region. A total of studies were identified, were searched from PubMed databases, were searched from Medline databases, 82 were from Web of science databases, and 14 were from others sources. After removing duplicates and review titles and abstracts, articles were excluded.

The remaining 41 articles were further examined and reviewed in full articles, 9 excluded due to methods, 2 insufficient data for detailed analysis, 2 not relevant, 3 reviews, 1 retracted, 1 not in humans. Finally, a subtotal of 23 original articles included in our meta-analysis Fig.


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A total of patients with autoimmune diseases and healthy controls were included in this study. The baseline characteristics of included studies are shown in Table 1. The age and sex were matched between patients with autoimmune diseases and healthy controls in each included study. The NOS for case-control studies was used to assess the quality of study and all quality scores of the enrolled original articles were higher than 5 score Table 1.

Heterogeneity was tested with the heterogeneity statistic Q and quantified using I 2. To evaluate stability of the results, we performed sensitivity analysis, which showed that the overall statistical significance does not change when any single study was omitted. Therefore, the current meta-analysis data is relatively reliable and credible Fig. This result showed that HMGB1 might play a crucial role in the pathogenesis of autoimmune diseases. HMGB1 is an important proinflammatory mediator and binds to cell surface receptors to induce inflammatory responses.

In addition, HMGB1 can translocate outside the cell in response to injuries by being actively secreted from activated immune cells or passively released from necrosis cells, extracellular HMGB1 can induce the release of proinflammatory mediators, which can result in highly increased serum levels of proinflammatory cytokines, and then cause the activation of immune system, as well as invasion by inflammatory cells, thereby prolonging and sustaining inflammatory processes. Wang et al [12] have demonstrated that plasma HMGB1 levels in AAV patients were significantly higher than those in normal controls and might reflect the disease activity.

Chen et al [30] findings show that HMGB1 might be a good laboratory index for the evaluation of disease activities and disease severity in AS patients.

INTRODUCTION

These results imply that the elevated serum HMGB1 levels may be a potential predictor in the disease activity of autoimmune diseases patients. Heterogeneity test results displayed the existence of significant heterogeneity among studies. Strong heterogeneity suggests that the validity of the meta-analysis is impaired, as the included studies reported inconsistent results.

We performed a subgroup analysis to investigate the potential influential factors for the results.

RCSB PDB - Gene View - HMGB1 - high mobility group box 1

Further studies with an adequate number of subjects according to different factors are needed. In addition, the strong heterogeneity may also be attributed to the two high-weight studies Ahn et al [16] and Kanakoudi et al [26] , both of which showed significantly higher HMGB1 levels than other studies. However, there exists some limitation in this meta-analysis which should be acknowledged.

First, there is the possible existence of biases. Although we performed a methodological assessment of those studies to avoid some selection biases, there was a highly significant heterogeneity among the 23 articles which may be attributed to age, gender, region, disease type and other residual confounding effect.

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Second, in this study we have not excluded patients with complicated autoimmune diseases such as SVV or SLE with renal involvement due to the limited studies we can include. Thirdly, if the original data were median and quartiles in selected articles, and may be cannot to acquire original data from the included studies. We transformed and calculated the data to gain the appropriate values.

Thus it may be lead to some errors of in our results.

Two high-mobility group box domains act together to underwind and kink DNA

Finally, studies published in languages other than English were not included, which may also indicate a language bias and affect the results in our study. Despite of have some limitations in our study, all the research methods were carried out on strict inclusion and exclusion criteria. Therefore, we obtained information may approximate the actual results. Further studies focusing on the underlying mechanisms of HMGB1 in autoimmune diseases are also needed.

Conceptualization: Nanfang Li. Formal analysis: Bin Zhu, Qing Zhu. Funding acquisition: Nanfang Li.

High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal.

Methodology: Qing Zhu, Ting Wu. Project administration: Nanfang Li. Writing — original draft: Bin Zhu. You may be trying to access this site from a secured browser on the server. Please enable scripts and reload this page. Two HMGB1 assays were used. Both demonstrated delayed kinetics for HMGB1 with high levels on inclusion that remained high throughout the study period.

This study, however, found no predictable correlation between serum levels of HMGB1 and severity of infection. We did quite unexpectedly find significantly lower levels of HMGB1 in nonsurvivors compared with survivors as measured by our main assay, but the other showed no difference between the two groups.


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Neither of these comparisons showed significant correlations for HMGB1. Conclusions: This is the first prospective study assessing the release over time of HMGB1 in a population of patients with sepsis, severe sepsis, or septic shock.