Coronavirus disease 2019 (COVID-19), which is caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused a global pandemic. The Omicron variant (B.1.1.529) was first discovered in November 2021 in specimens collected from Botswana, South Africa. Omicron has become the dominant variant worldwide, and several sublineages or subvariants have been identified recently. Compared to those of other mutants, the Omicron variant has the most highly expressed amino acid mutations, with almost 60 mutations throughout the genome, most of which are in the spike (S) protein, especially in the receptor-binding domain (RBD). These mutations increase the binding affinity of Omicron variants for the ACE2 receptor, and Omicron variants may also lead to immune escape. Despite causing milder symptoms, epidemiological evidence suggests that Omicron variants have exceptionally higher transmissibility, higher rates of reinfection and greater spread than the prototype strain as well as other preceding variants. Additionally, overwhelming amounts of data suggest that the levels of specific neutralization antibodies against Omicron variants decrease in most vaccinated populations, although CD4+ and CD8+ T-cell responses are maintained. Therefore, the mechanisms underlying Omicron variant evasion are still unclear. In this review, we surveyed the current epidemic status and potential immune escape mechanisms of Omicron variants. Especially, we focused on the potential roles of viral epitope mutations, antigenic drift, hybrid immunity, and “original antigenic sin” in mediating immune evasion. These insights might supply more valuable concise information for us to understand the spreading of Omicron variants.

Our previous work has demonstrated that the tetraspan MS4A6D interacts with MHC-II to be a complex that promotes macrophage activation (Mol Immunol. 2023; 160: 121-132), however, the exact role of MS4A6D in controlling macrophage-derived inflammation is still poorly understood. Here, we showed that Ms4a6d-deficient (Ms4a6d-/-) mice manifested a lower level of footpad swelling induced by subcutaneous injection of 100 μL of 1% Carrageenan (CGN, w/v) plus CaCl2 (50 mM), a phenomenon that is similar to Nlrp3-/-, Casp-1-/-, and Ilr1-/- mice. Mechanistically, F4/80+ macrophages infiltrated in the footpad tissues of the Ms4A6d-/- mice was significantly lower than that of the WT littermates, leading to dramatically lower levels of proIL-1β in vivo. Moreover, macrophages from Ms4a6d-/- mice also showed a dramatical reduction of Il-1β secretion following NLRP3 inflammsome activation in vitro. Interestingly, both Ms4a6dC237G mutant (Interruption of MS4A6D homodimerization) and Ms4a6dY241G mutant (deletion of heITAM motif) mice also significantly inhibited CGN-induced footpad swelling due to lower levels of Il-1β secretion in vivo. Collectively, MS4A6D aggravates CGN-induced footpad swelling in mice by enhancing NLRP3 inflammasome in macrophages and inducing the release of IL-1β, indicating that MS4A6D promotes the progression of acute inflammation.

Neurogenic heterotopic ossification（NHO） is a pathological phenomenon following central nervous system injuries, i.e.,new bones are formed in muscles, tendons, and joint surroundings where no bones exist initially. NHO may result in severe joint pain, deformity, and even complete ankylosis, which seriously affects the patients’ quality of life. Therefore, the early diagnosis and treatment of NHO is very important. This article systematically reviews the prevention, surgical timing and possible therapeutic targets as well as potential biomarkers for NHO,in order to provide new ideas for its diagnosis and treatment.

创伤性脑损伤(traumatic brain injury,TBI)合并四肢骨折是常见的多发伤类型之一.许多临床和基础研究表明,相较于单纯肢体骨折,TBI可以加速骨折愈合的速度,在骨折端形成大量骨痂,但其具体机制目前仍未阐明.探讨TBI加速骨折愈合的机制,可能为临床治疗骨折愈合不良和骨不连提供新的思路.本文围绕TBI后非编码RNA、信号素3A、神经肽、巨噬细胞和激素调节在骨折愈合中的影响作一综述,重点介绍其相关机制.

It is commonly observed that patients with bone fracture concomitant with traumatic brain injury (TBI) had significantly increased fracture healing, but the underlying mechanisms were not fully revealed. Long non-coding RNAs (lncRNAs) are known to play complicated roles in bone homeostasis, but their role in TBI accelerated fracture was rarely reported. The present study was designed to determine the role of lncRNAs in TBI accelerated fracture via transcriptome sequencing and further bioinformatics analyses. Blood samples from three fracture-only patients, three fracture concomitant with TBI patients, and three healthy controls were harvested and were subsequently subjected to transcriptome lncRNA sequencing. Differentially expressed genes were identified, and pathway enrichment was performed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. High-dimensional data visualization by self-organizing map (SOM) machine learning was applied to further interpret the data. An xCell method was then used to predict cellular behavior in all samples based on gene expression profiles, and an lncRNA–cell interaction network was generated. A total of 874 differentially expressed genes were identified, of which about 26% were lncRNAs. Those identified lncRNAs were mainly enriched on TBI-related and damage repair-related pathways. SOM analyses revealed that those differentially expressed lncRNAs could be divided into three major module implications and were mainly enriched on transcriptional regulation and immune-related signal pathways, which promote us to further explore cellular behaviors based on differentially expressed lncRNAs. We have predicted that basophils, CD8+ T effector memory cells, B cells, and naïve B cells were significantly downregulated, while microvascular endothelial cells were predicted to be significantly upregulated in the Fr/TBI group, was the lowest and highest, respectively. ENSG00000278905, ENSG00000240980, ENSG00000255670, and ENSG00000196634 were the most differentially expressed lncRNAs related to all changes of cellular behavior. The present study has revealed for the first time that several critical lncRNAs may participate in TBI accelerated fracture potentially via regulating cellular behaviors of basophils, cytotoxic T cells, B cells, and endothelial cells.

Hyperactivation of the NLRP3 inflammasome contributes to the pathogenesis of multiple diseases, but the mechanisms underlying transcriptional regulation of Nlrp3 remain elusive. We demonstrate here that macrophages lacking V-set and immunoglobulin domain-containing 4 (Vsig4) exhibit significant increases in Nlrp3 and Il-1β transcription, caspase-1 activation, pyroptosis, and interleukin-1β (IL-1β) secretion in response to NLRP3 inflammasome stimuli. VSIG4 interacts with MS4A6D in the formation of a surface signaling complex. VSIG4 occupancy triggers Ser232 and Ser235 phosphorylation in MS4A6D, leading to activation of JAK2-STAT3-A20 cascades that further results in nuclear factor κB suppression and Nlrp3 and Il-1β repression. Exaggerated NLRP3 and IL-1β expression in Vsig4-/- mice is accountable for deleterious disease severity in experimental autoimmune encephalomyelitis (EAE) and resistance to dextran sulfate sodium (DSS)-induced colitis. The agonistic VSIG4 antibodies (VG11), acting through NLRP3 and IL-1β suppression, show significant therapeutic efficacy in mouse EAE. These findings highlight VSIG4 as a prospective target for treating NLRP3-associated inflammatory disorders.

To investigate the expression of soluble B7-H3 (sB7-H3) in the peripheral blood of patients with traumatic brain injury (TBI) combined with fracture,fracture only,or TBI only,and study the effects of sB7-H3 on differentiation of mesenchymal stem cells (MSCs) to osteoblast,the expression of sB7-H3 and fracture healing marker Cbfa1 in peripheral blood of patients with TBI combined with fracture,fracture only,TBI and normal volunteers were detected by ELISA,and the effect of recombinant B7-H3 protein on osteogenic differentiation of MSCs were examined by Alizarin red and real-time PCR.Data showed that the expression of sB7-H3 in patients with TBI combined with fracture or TBI were significantly higher than that in fracture only and normal volunteers.Moreover,the concentration of sB7-H3 in peripheral blood was correlated with the severity of traumatic brain injury.And recombinant B7-H3 protein could promote the differentiation of MSCs into osteoblasts in a dose dependent manner.In conclusion,the elevated sB7-H3 in peripheral blood caused by TBI promotes fracture healing.

Bladder cancer is one of most common malignant cancer. Although previous studies have found abnormal expression of B7-H3 in human bladder cancer tissues, the exact role and molecular mechanism of B7-H3 in bladder cancer remain unknown. In this study, we first detected the expression of B7-H3 in human bladder cancer samples and cell lines, and analyzed its correlations with clinicopathological pathological parameters. Next, siRNAs or overexpression plasmids of B7-H3 were transfected into T24 or 5637 cells, and cell proliferation, apoptosis, migration and invasion were analyzed via CCK-8, colony formation, flow cytometry and transwell assays, protein expression levels were determined by western blotting. The results presented here showed B7-H3 was upregulated in bladder cancer samples compared with normal tissues, and the expression level was correlated with local invasion status. B7-H3 did not affect cell proliferation and apoptosis, but cell migration and invasion were changed through the regulation of matrix metalloproteinase (MMP) 2/9. Knockdown of B7-H3 resulted in decreased activity of the STAT3 and PI3K/Akt pathways, and the Akt served as an upstream regulator of the STAT3. Our results suggest that the overexpression of B7-H3 promotes the migration and invasion of human bladder cancer cells through the PI3K/Akt/STAT3 signaling pathway.

Severe trauma can promote the release of a large amounts of cytokines by starting the nerve-endocrine-immune system,then,induce systemic inflammatory response syndrome (SIRS).At the same time,the cytokines cause cascade amplification and promote SIRS developing by complex interactive networks,eventually leading to multiple organ dysfunction syndrome (MODS) and failure (MOF).At present,there are many researches about the treatment of cytokines,including the treatment of cytokine antagonists,Gene therapy,blood purification therapy,etc.This article will describe the significance of the changes of the main cytokines after trauma,and briefly introduce the treatment of cytokines.

目的 观察血栓通对颅外伤合并多发性肋骨骨折患者的临床疗效.方法 66例颅外伤合并多发性肋骨骨折患者随机分为对照组33例和试验组33例.2组均实施手术纠正及持续吸氧、降颅压、神经营养支持、纠正水电解质紊乱、对症治疗等治疗.试验组在此基础上,静脉滴注血栓通注射液5 mL,溶于5％葡萄糖溶液250 mL,每日1次,持续14 d.比较2组患者治疗前、治疗7,14 d后疼痛评分、血氧饱和度变化和神经功能缺损程度评分;根据患者病情分为Ⅰ、Ⅱ、Ⅲ级,比较各级患者呼吸机使用时间、止痛药使用时间及住院时间.结果 治疗7,14 d后,试验组的疼痛视觉模拟评分(VAS)分别为(2.33±0.51),(1.20±0.38)分,对照组的VAS分别为(7.05±1.39),(2.81±0.40)分;试验组神经功能缺损程度评分量表(NDS)评分分别为(10.70±2.99),(8.06±3.38)分,对照组的NDS评分分别为(15.84±4.62),(11.29±2.58)分,差异有统计学意义(P＜0.05).治疗7,14 d后,试验组的动脉血氧饱和度(Sp02)分别为(90.36±3.55)％,(95.52±4.07)％;对照组的SpO2分别为(89.81±3.42)％,(94.71±3.96)％,2组与治疗前相比,差异均有统计学意义(均P＜0.05).试验组Ⅰ、Ⅱ、Ⅲ级患者呼吸机使用时间分别为0,(1.13±0.96),(4.02±3.70)d;对照组Ⅰ、Ⅱ、Ⅲ级患者呼吸机使用时间分别为0,(4.59±3.05),(7.96±6.13)d;试验组Ⅰ、Ⅱ、Ⅲ级患者止痛药使用时间分别为(2.09±0.58),(4.71±0.83),(7.09±1.25)d,对照组Ⅰ、Ⅱ、Ⅲ级患者止痛药使用时间分别为(4.31±1.07),(8.20±3.55),(13.26±5.81)d;试验组Ⅰ、Ⅱ、Ⅲ级患者住院时间分别为(10.69±3.75),(15.36±8.22),(18.31±5.07)d,对照组Ⅰ、Ⅱ、Ⅲ级患者住院时间分别为(17.26±3.58),(19.39±5.42),(30.05±2.44)d,2组差异有统计学意义(P＜0.05).2组均未发生药物不良反应.结论 血栓通能够有效改善颅外伤合并多发性肋骨骨折患者临床症状,促进其神经功能及机体状态的恢复,有助于缩短住院时间和止痛药物用量,对患者预后质量的改善具有积极作用.

Objective To analyze the related factors of foot blisters caused by long-distance weight-bearing march and to explore the pathogenesis of foot blisters to provide a useful way for the prevention and treatment.Methods After the 300 km march,counted the number who had accomplished the march,and then recorded the number of foot blisters,location of blisters,and abrasion of sole.Collected the data of gender,age,body mass index (BMI),hand dominance,and whether had bliters before the march through questionnaire.And the data were coded for analysis with SPSS 13.0 statistical package.Results The 7 cases who complete the whole march and 17 cases who already had foot blisters before the march were ruled out of the final statistics.Among the remaining 590 cases,there were 554 cases (93.9%)suffered from foot blisters.And there were 1 282 blisters in total,among which the plantar blisters occupied 98% (1 257 cases).The analysis showed that the incidence of foot blisters had no significant correlation with gender,left/right foot,hand dominance,BMI and age.The predilection sites of blisters were the second and third metatarsals (28.2%),the hallux (21.3%),the fifth metatarsal (18.1%),and the calcaneus (15.8%)of the left foot.The predilection sites of blisters were the second and third metatarsals (33.3%),the hallux (22.4%),the fifth metatarsal (18.6%),and the calcaneus (14.5%)of the right foot.In terms of the abrasion of sole,the lateral heel was worn out the most (34.6% on the left and 34.2% on the right).Conclusion The study confirmed that the incidence of foot blisters had no significant correla-tion with gender,left/right foot,hand dominance,BMI and age,which may be affected by the particularity of this march.Most of the foot blisters occurred in the planta,and the predilection sites of blisters were in accord with sites of of the abrasion of sole and the distribution of plantar shear force,which demonstrated the shear force is the most critical factor on the pathogenesis of foot blisters.

Objective To evaluate the effect of pre-emptive analgesia on pain and inflammation control in patients with severe multiple trauma.Methods Severe multiple trauma patients treated in the emergency department from September 2014 to December 2014 were prospectively included based on the inclusion criteria including injury severity score (ISS) of 16 to 25,Glasgow Coma Scale (GCS) ≥ 13 and visual analogue scale (VAS) ≥ 4.The patients were assigned to pre-emptive analgesia group,traditional analgesia group and non-analgesia group,according to the random number table.Pre-emptive analgesia group had patient-controlled intravenous analgesia (PCIA) with sufentanil and tramadol on admission.Traditional analgesia group were administered intramuscular pethidine or subcutaneous morphine for temporary analgesia when the pain could not be tolerated.Non-analgesia group received no analgesia.VAS,systemic inflammatory response syndrome (SIRS) score and serum interleukin (IL)-6 concentration were compared among the groups on admission day,24,48,72,120,168 and 240 h after admission.Results Fifty-seven patients (46 males and 11 females) were included,and age was (39.61 ± 12.05)years.There were 18 patients in pre-emptive analgesia group,20 patients in traditional analgesia group,and 19 patients in non-analgesia group.Comparison between pre-emptive analgesia,traditional analgesia and non-analgesia groups showed no significant differences on admission with respect toVAS [(6.5±1.5),(6.6±1.4),(6.4 ±1.4)points],SIRS [(3.3±0.7),(3.4±0.6),(3.4±0.8) points] and IL-6 concentration [(109.2 ± 47.9),(99.9 ± 44.3),(106.3 ± 50.0) ng/L] (P ＞0.05).Compared to traditional analgesia and non-analgesia groups,VAS and SIRS score in pre-emptive analgesia group differed significantly at 24,48,72,120,168 and 240 h after admission,and IL-6 in pre-emptive analgesia group differed significantly at 48,72,120,168 and 240 h after admission (all P ＜0.05).VAS,SIRS score and IL-6 concentration declined faster in pre-emptive analgesia group than other two groups (P ＜ 0.05),while there were no significant differences between traditional analgesia and nonanalgesia groups (P ＞ 0.05).Positive correlation was noted between VAS and SIRS score,and between VAS and t IL-6 concentration (P ＜ 0.05).Conclusion Pre-analgesia provides quick and effective pain relief and attenuate excessive systemic inflammation response that contributes to stabilization and recovery of the severe multiple trauma patients.

OBJECTIVE:To design a specific polyclonal antibody against Deinagkistrodon acutus venom (DA-pAb) by immunizating New Zealand white rabbits.RESULTS:The IgG fraction was purified by affinity chromatography, and specific antibodies were purified by immunoaffinity chromatography. Polyclonal antibodies were subjected to ELISA and western blotting to evaluate their immune reactivity. We identified the mimotopes by screening a phage display 12-mer peptide library against D. acutus venom. After three rounds of biopanning with DA-pAb, 30 positive clones were identified. Eighteen phage clones were sequenced, and their corresponding amino acid sequences were deduced. Additional immunoassays with the peptides and DA-pAb identified five sequences as possible epitopes. Recombinant antigens synthesized with the five epitopes were used for the immunization of BALB/c mice.CONCLUSION:The antibodies induced by these peptides recognized the recombinant antigen and D. acutus venom and protected mice against the hemorrhagic effects of the venom.

目的:分析某高校同质性群体在5 km负重比赛中热射病发病相关因素,提出预防建议;分析本次针对批量集中发生热射病的救治情况,总结救洽经验.方法:赛后根据热射病发病情况,将参赛人员分为热射病组及非热射病组,对参赛人员进行问卷调查,内容包括一般情况、热射病可能相关因素等,予计量资料t检验,计数资料x2检验,热射病可能相关因素Logistic回归分析;对热射病患者行早期综合救治,院内动态监测生命体征及格拉斯哥昏迷(GCS)评分,记录每位患者ICU及总住院时间,随访观察预后状况.结果:共11例热射病患者,热射病组与非热射病组间年龄、体重指数、籍贯比较差异无统计学意义;比赛经验与热适应是热射病的保护因素,其对热射病的OR值分别为0.030、0.015,冲刺突然加速、赛前不适情绪、赛前躯体不适是热射病的危险因素,OR值分别为:73.511、99.235、453.769;热射病患者经早期综合救治后,患者生命体征及GCS评分在1h内明显好转,6h内全部恢复正常,平均ICU住院时间及总住院时间分别为(14.18±7.24)h、(76.32±14.4)h,所有患者痊愈出院,无后遗症.结论:本群体高度同质性;热适应等措施可有效预防热射病的发生;越早对热射病患者行综合性救治,预后越好.

Although acute mountain sickness (AMS) has long been recognized, little is known about this condition to date. The current study was conducted to explore changes in the metabolomic profiles of AMS patients and to further assess the potential of using these changes for the diagnosis of AMS.Plasma samples from 12 patients with AMS and 12 individuals without AMS were collected and used for further bioinformatics analysis by gas chromatography-mass spectrometry (GC-MS). The following analytical methods were used: gas chromatography-mass spectrometry data preprocessing, principal components analysis, partial least squares-discriminant analysis, model validation, orthogonal partial least squares-discriminant analysis, and the screening and identification of differences in metabolites.The results revealed a significant difference between the subjects with AMS and those in the control group. Compared with plasma from the controls, plasma from the AMS patients contained significantly increased hypoxanthine, cysteinylglycine, D-arabitol, L-allothreonine, 2-ketobutyric acid, and succinate semialdehyde.The identification of metabolomic changes may be useful for the diagnosis of AMS in the future and may lay the foundation for further study of AMS pathogenesis.

Acute mountain sickness (AMS) is the most common high altitude illnesses experienced during rapid ascent to a higher altitude without prior acclimation. It is mainly characterized by a headache which may be accompanied with nausea, vomiting, anorexia, dizziness, lethargy, fatigue, and sleep disturbance. If not diagnosed and treated in a timely manner, AMS can develop into deadly high altitude pulmonary edema or high altitude cerebral edema. In the previous studies of individual variation in susceptibility to AMS, arterial oxygen saturation (SO2) was identified as being associated with AMS. However, other studies have reported no association between AMS and arterial oxygen saturation. In this study, the association between SO2 and AMS was assessed through a meta-analysis of published data. The literature databases PubMed, Web of Science, LWW, Science Direct, and Embase were queried for papers published before 15 April 2014. A fixed-effects model and a random-effects model were applied (Revman 5.0) on the basis of heterogeneity, and the study quality was assessed in duplicate. Twelve studies with 614 AMS patients and 1,025 control subjects were analyzed. There was a significant association with differences in SO2 and the risk of developing AMS. SO2 values are associated with AMS incidence.

BACKGROUND:Programmed death-1 (PD-1, Pdcd1)-deficient mice develop different types of autoimmune diseases depending on the mouse strain but its role in uterus development has not been reported.METHODS:In this study, the expression of PD-1 and its ligands, PD-L1 and PD-L2, in uterine tissues from aged WT mice in a 129svEv-Brd background was analyzed by immunohistochemistry and the uterine morphology between WT and PD-1-/- mice was compared by hematoxylin and eosin staining.RESULTS:The aged PD-1-/- female mice in a 129svEv-Brd rather than Balb/c background develop endometrial hyperplasia. H&E staining showed an increase in the number of glands, neovascularization and an extremely large luminal cavity in aged PD-1-/- uteri. Immunohistochemical assay showed that the expression of PD-1 was observed in glandular/luminal epithelium and cells infiltrating the stroma. Fluorescent double staining demonstrated that PD-1 expresses on CD68+ macrophages, CD3+ T cells, CD16+ monocytes, CD56+ NK cells and CK-18+ epithelial cells, respectively. Additionally, PD-1 co-expresses with vascular endothelial growth factor (VEGF), and PD-1 deficiency resulted in an accumulation of glandular/luminal epithelium derived VEGF, which accelerates the expression of the proliferation-associated protein, proliferating cell nuclear antigen (PCNA), and thus potentially lead to epithelial proliferation in aged PD-1-/- uteri.CONCLUSIONS:These findings showed that PD-1 deficiency augments luminal epithelial cell proliferation probably through induced VEGF secretion, suggesting PD-1 plays an important role in controlling the growth and differentiation of the uterine epithelium.VIRTUAL SLIDES:The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/5809067461223905.

Signals from the T cell immunoglobulin and mucin-domain (TIM)-containing molecules have been demonstrated to be involved in regulating the progress of carcinoma. However, the expression and anatomical distribution of TIMs in Langerhans cell sarcoma (LCS), which is a rare malignancy derived from dendritic cells of the epidermis, has yet to be determined. In this study, the expression of TIM-1, TIM-3 and TIM-4 in LCS samples were detected by immunohistochemistry. Our results showed that these three molecules were found in LCS sections. At the cellular level, these molecules were found on the cell membrane and in the cytoplasm. Immunofluorescence double-staining demonstrated that these TIMs were co-expressed with Langerin, a potential biomarker for detecting LCS. In addition, TIM-1 was also expressed on CD68(+) macrophages and CK-18(+) epithelial cells, while TIM-3 and TIM-4 were expressed on all cell types investigated, including CD3(+)T cells, CD68(+) macrophages, CD11c(+) dendritic cells, CD16(+) NK Cells, CD31(+) endothelial cells and CK-18(+) epithelial cells. Interestingly, TIMs were also co-expressed with some members of the B7 superfamily, including B7-H1, B7-H3 and B7-H4 on sarcoma cells. Our results clearly showed the characteristic expression and anatomical distribution of TIMs in LCS, and a clear understanding of their functional roles may further elucidate the pathogenesis of this carcinoma and potentially contribute to the development of novel immunotherapeutic strategies.

Hepatitis B virus (HBV) infection is a major public health problem, and HBV-related acute-on-chronic liver failure (HBV-ACLF) has an extremely poor prognosis due to a lack of understanding of pathogenesis as well as a lack of effective treatments. Signals from the inhibitory receptor programmed death-1 (PD-1) have been demonstrated to be involved in regulating the pathogenesis of infectious diseases. However, the expression of PD-1 and its ligands in HBV-ACLF patients has yet to be evaluated. In this study, the expression of PD-1 and its ligands, PD-L1 and PD-L2, in liver biopsies from HBV-ACLF as well as chronic hepatitis B (CHB) patients were analyzed by immunohistochemistry. The results showed that all three molecules were observed in the HBV-ACLF samples and their levels were significantly higher than they were in CHB. Immunofluorescence double-staining showed that PD-1 was found on CD3(+), CD8(+) T cells, CD56(+) NK cells, CD68(+) macrophages, CK-18(+) epithelial cells, and CD16(+) monocytes. The PD-L1 expression was observed on all cell types detected and the PD-L2 was chiefly on CK-18(+) epithelial cells and CD31(+) endothelial cells. Interestingly, high levels of virus-induced procoagulant molecule fibrinogen-like protein 2 (FGL2) were observed in liver sections from HBV-ACLF, and PD-L1 and PD-L2 expression was also observed on FGL2(+) cells in these patients. Our combined results suggest that the expression of PD-L1 and PD-L2 may be biomarkers to identify and diagnose ACLF, and a clear understanding of their functional roles should further elucidate the pathogenesis of this disease.