OBJECTIVE:To investigate whether peritumoral electroacupuncture (EA) suppresses tumor growth viaCD8+ T cell infiltration mediated by sympathetic nervous system (SNS) regulation. METHODS:Utilizing a mouse model of triple-negative breast cancer (TNBC), the SNS was activated through chronic restraint stress (CRS); chemical sympathetic denervation was induced by 6-hydroxydopamine (6-OHDA). The anti-tumor and immune regulatory effects of EA were evaluated by multidimensional methods, including in vivobioluminescence imaging, flow cytometry, immunofluorescence, and enzyme-linked immunosorbent assay. RESULTS:Peritumoral EA decreased the volume and weight of tumors within 22 d after the implantation. Intratumoral CD8+ T cells significantly increased after EA. C-C motif chemokine ligand 5, as a chemokine that recruits effector T cells to the tumor microenvironment, also up-regulated. Meanwhile, EA reduced intratumoral sympathetic innervation and norepinephrine level. Subsequently, we found CRS significantly accelerates tumor growth and reduces the density of CD8+ T cell infiltration. However, EA reversed the tumor-promoting effect and immune suppression caused by CRS effectively. Furthermore, chemical sympathetic ablation with 6-OHDA revealed that the anti-tumor effect of EA was dependent on sympathetic integrity, as the ablation impaired both tumor-suppressing effect and CD8+ T cell recruitment mediated by EA. CONCLUSION:EA enhances anti-tumor immunity through SNS emphasizing the effective remodeling of the tumor immune microenvironment in mice with TNBC by neuro-immune interactions.

The triggering receptor expressed on myeloid cells 2 (TREM2) is an immune receptor that affects cellular phenotypes by modulating phagocytosis and metabolism, promoting cell survival, and counteracting inflammation. Its role in renal injury, in particular, unilateral ureteral obstruction (UUO) or ischemia-reperfusion injury (IRI)-induced renal injury remains unclear. In our study, WT and Trem2−/− mice were employed to evaluate the role of TREM2 in renal macrophage infiltration and tissue injury after UUO. Bone marrow-derived macrophages (BMDM) from both mouse genotypes were cultured and polarized for in vitro experiments. Next, the effects of TREM2 on renal injury and macrophage polarization in IRI mice were also explored. We found that TREM2 expression was upregulated in the obstructed kidneys. TREM2 deficiency exacerbated renal inflammation and fibrosis 3 and 7 days after UUO, in association with reduced macrophage infiltration. Trem2−/− BMDM exhibited increased apoptosis and poorer survival compared with WT BMDM. Meanwhile, TREM2 deficiency augmented M1 and M2 polarization after UUO. Consistent with the in vivo observations, TREM2 deficiency led to increased polarization of BMDM towards the M1 proinflammatory phenotype. Mechanistically, TREM2 deficiency promoted M1 and M2 polarization via the JAK-STAT pathway in the presence of TGF-β1, thereby affecting cell survival by regulating mTOR signaling. Furthermore, cyclocreatine supplementation alleviated cell death caused by TREM2 deficiency. Additionally, we found that TREM2 deficiency promoted renal injury, fibrosis, and macrophage polarization in IRI mice. The current data suggest that TREM2 deficiency aggravates renal injury by promoting macrophage apoptosis and polarization via the JAK-STAT pathway. These findings have implications for the role of TREM2 in the regulation of renal injury that justify further evaluation.

Renal fibrosis is the common final pathway of progressive renal diseases, in which the macrophages play an important role.ELISA was used to detect CD5 antigen-like (CD5L) in serum samples from end-stage renal disease (ESRD), as well as in mice serum with unilateral ureteral occlusion (UUO). Recombinant CD5L was injected into UUO mice to assess renal injury, fibrosis, and macrophage infiltration.The expression of CD5L was significantly upregulated in the serum of patients with ESRD and UUO mice. Histological analysis showed that rCD5L-treated UUO mice had more severe renal injury and fibrosis. Furthermore, rCD5L promoted the phenotypic transfer of monocytes from Ly6Chigh to LyC6low. RCD5L promoted TGF-β signaling pathway activation by promoting Smad2/3 phosphorylation. We used Co-IP to identify HSPA5 interact with CD5L on cell membrane could inhibit the formation of the Cripto/HSPA5 complex, and promote the activation of the TGF-β signaling pathway. The CD5L antibody could reduce the degree of renal fibrosis in UUO mice.

There is a commonality between jingjin (muscle region of meridian) and the fascial network for coordinating the balance in the body. The occurrence and the progression of tumor may disrupt the overall coordination between the fascial network and jingjin directly or indirectly, thereby, the impairment of this coordination may result in cancer pain. Rooted on the theory of overall balance of the fascial network, and combined with understanding of pain in jingjin theory, professor HUANG Jin-chang emphasizes the importance of "relaxing the knot" in treatment of cancer pain. It is recommended to select the fascia reaction point as the target point, in accordance with the principle of balance adjustment and apply various acupuncture and moxibustion therapies, such as Fu's subcutaneous needling, small-needle scalpel therapy, fire needling, and moxibustion.

Disulfide bond A oxidoreductase-like protein (DsbA-L) drives acute kidney injury (AKI) by directly upregulating the expression of voltage-dependent anion-selective channels in proximal tubular cells. However, the role of DsbA-L in immune cells remains unclear. In this study, we used an LPS-induced AKI mouse model to assess the hypothesis that DsbA-L deletion attenuates LPS-induced AKI and explore the potential mechanism of DsbA-L action. After 24 hours of LPS exposure, the DsbA-L knockout group exhibited lower serum creatinine levels compared to the WT group. Furthermore, peripheral levels of the inflammatory cytokine IL-6 were decreased. Transcriptomic data analysis revealed a significant down-regulation in the IL-17 and tumor necrosis factor pathways in DsbA-L knockout mice following LPS induction. Metabolomic analysis suggested that arginine metabolism was significantly different between the WT and DsbA-L knockout groups after LPS treatment. Notably, the M1 polarization of macrophages in the kidneys of DsbA-L knockout AKI mice was significantly reduced. Expression of the transcription factors NF-κB and AP-1 was downregulated after DsbA-L knockout. Our results suggest that DsbA-L regulates LPS-mediated oxidative stress, promotes M1 polarization of macrophages, and induces expression of inflammatory factors via the NF-κB/AP-1 pathway.

Background Danggui Buxue Decoction (DBD) is a traditional Chinese medicine prescription, which has the functions of benefiting Qi, generating blood and regulating the immune system. At present, various clinical reports suggest that DBD has some efficacy in Rheumatoid arthritis (RA), but its mechanism of action is still unclear. Thus, the present study explored mechanism of this preparation on RA. Methods The effect of DBD was evaluated by tumor necrosis factor (TNF)-α-induced Human fibroblast-like synoviocyte of rheumatoid arthritis (HFLS-RA) cell model and collagen-induced arthritis (CIA) rat model, respectively. Inflammatory factors including TNF-ɑ, IL-1β, IL-6 and IL-10 in the culture supernatants or rat serum were measured using ELISA. The related indexes including fur luster, mental state and activity of rat and the symptoms including swelling and deformation of toes and ankles were also measured. Results In vitro results showed that DBD cannot only inhibit the proliferation of HFLS-RA cells but also reduce the levels of pro-inflammatory factors while increasing the level of anti-inflammatory factors. Similar results were obtained from in vivo experiments. Rats receiving DBD showed a decrease in the severity of rheumatoid arthritis in rat models. Moreover, the protein levels of c-myc and β-catenin decreased significantly, while the protein level of SFRP4 increased, which indicated that DBD might inhibit the inflammatory reaction by regulating Wnt/β-catenin signaling pathway, thus alleviating the symptoms of RA. Conclusion Our findings not only provide insights for understanding the molecular mechanism of DBD in treating RA, but also provide the theoretical basis for further clinical prevention and treatment.

声音嘶哑为甲状腺结节热消融术后的常见并发症,认为其乃因火毒直中咽喉,火毒、气结、痰湿、瘀血相互胶结,痹阻喉窍,致声门不利,金实不鸣.如未及时施治,病情进展,可使脏腑功能失调而加重局部病邪胶结.临床根据患者病程长短进行分期辨证,结合伴随症状,认为急性期多为实证,且患者热象明显,辨证多以痰火阻窍为主;亚急性期辨证多属气滞血瘀夹痰湿;慢性期为虚实夹杂或见虚证,辨证多属阴虚火旺或气阴两虚.治则以泻火解郁化痰、行气活血祛湿为主,兼以养阴益气清热、育阴潜阳熄风.处方以升降散为基本组方,随症加减,并辅金津、玉液刺血,颈前横纹针刺和患处中药外敷等外治法.全身治疗与局部治疗相互配合,针药并用,饮食与情绪调护并重,则喑哑自愈.

The pathogenesis of lung metastases from renal carcinoma is the deficiency of both the Lung and the Kidney, blockage of Sanjiao, and failure in eliminating Phlegm and Dampness.Renal carcinoma is originated in Kidney deficiency, in which deficiency of Kidney Yin negatively affects the Kidney Yang, which weakens the Qi transformation function of the Kidney.When the function of Qi, Blood, and body Fluid in the Sanjiao is abnormal, and the Lungs cannot be nourished by Qi, Blood, and body Fluid, resulting in insufficient Lung Qi and Yin over time.Deficiency of both Qi and Yin causes the Lung′s failure in clearing and descending, resulting in the inability of the body Fluid in the Lungs to disperse, and then the Phlegm, Water, and Dampness stay in the Lungs and get accumulated over time.The Kidney governs bones, and the Shaoyang governs the periosteum.Because renal carcinoma is originally caused by the loss of Kidney essence, which fails in nourishing the bones, and the bones that lose their nourishment are easily attacked by pathogenic Qi.At the same time, the power of Shaoyang to support the movement of Qi, Blood, and body Fluid comes from Kidney.If the kidney is deficient, the pivot of Shaoyang will be unfavorable, and Phlegm, Dampness and blood stasis will generate inward and stay in the fascia of the deficient bones, and get accumulated over time.Lung and bone metastasis of renal carcinoma is closely related to "Shaoyang belonging to Kidney and Kidney being connected to Lung so the two Zang are closely connected" and "Shaoyang governing the bone".Therefore, in treatment of renal carcinoma dredging and benefiting Shaoyang while nourishing the Kidney and strengthening the foundation should be paid special attention to.Clinically, it should be based on the whole, pay attention to the local area, by combining dredge method and tonic method, and the following priscriptions should be chosed: modified Liuwei Dihuang Pill combined with Chaihu Dayuan Drink, Haibai Baidong Decoction for lung metastases from renal carcinoma.Modified Guifu Dihuang Pills combined with Chaiqin Decoction and Yanghe Decoction were used for bone metastasis of renal carcinoma.In addition, emotional care and daily diet should also be emphasized.

Objective: To investigate the application effect of extracorporeal membrane oxygenation (ECMO) in patients with severe acute respiratory distress syndrome (ARDS) caused by Pneumocystis jirovecii pneumonia (PJP) after kidney transplantation. Methods: This is a case series on 10 kidney transplant recipients with severe ARDS caused by PJP at the People’s Hospital of Zhengzhou, who were enrolled as the case group. A total of 17 cases of PJP diagnosed with severe ARDS without ECMO were selected as the control group. The timing and mode of ECMO support and treatment complications were summarized. The primary aim of this study was mortality and secondary was imaging and complications. Results: The enrolled patients’ oxygenation index before the start of ECMO ranged from 25 to 92, and the time from admission to the start of ECMO was 1–17 days, with an average of 5.56 days. In the case group, one patient died of hemorrhagic shock due to abdominal hemorrhage, but the other nine patients were successfully weaned from ECMO. Of these patients, one died due to sepsis following weaning. The survival rate in the case group was 80.0% (8/10), and the survival rate in the control group was 35.29% (6/17). The vein–vein ECMO support time in the nine successfully weaned patients in the case group ranged from 131 to 288 h, with an average of 215.5 h. Of the eight patients who survived, deterioration of renal function after transplantation occurred in two patients, but no fatal complications occurred. Conclusion: Overall, Patients with severe ARDS caused by postoperative PJP infection following kidney transplantation have a poor prognosis. The mortality was lower in patients who were treated with ECMO compared to standard care.

Sepsis-associated encephalopathy (SAE) is a common and severe complication of sepsis. The cognitive dysfunction that ensues during SAE has been reported to be caused by impairments of the hippocampus. Microglia serves a key role in neuroinflammation during SAE through migration. Forkhead box C1 (Foxc1) is a member of the forkhead transcription factor family that has been found to regulate in cell migration. However, the role of Foxc1 in neuroinflammation during SAE remains unknown. In the present study, the mechanistic role of Foxcl on microglial migration, neuroinflammation and neuronal apoptosis during the occurrence of cognitive dysfunction in SAE was investigated. A microglia-mediated inflammation model was induced by LPS in BV-2 microglial cells in vitro, whilst a SAE-related cognitive impairment model was established in mice using cecal ligation and perforation (CLP) surgery. Cognitive function in mice was evaluated using the Morris Water Maze (MWM) trial. Lipopolysaccharide (LPS) treatment was found to trigger BV-2 cell migration, inflammation and neuronal apoptosis. In addition, CLP surgery induced cognitive injury, which was indicated by longer latencies and shorter dwell times in the goal quadrant compared with those in the Sham group in the MWM trial. LPS treatment or CLP induction decreased the expression of Foxc1 and inhibitor of NF-kappa B (I kappa B alpha) whilst increasing that of p65, IL-1 beta and TNF-alpha. After Foxc1 was overexpressed, the cognitive dysfunction of mice that underwent CLP surgery was improved, with the expression of I kappa B alpha also increased, microglial cell migration, the expression of p65, IL-1 beta and TNF-alpha and neuronal apoptosis were all decreased in vivo and in vitro, which were in turn reversed by the inhibition of I kappa B alpha in vitro. Overall, these results suggest that the overexpression of Foxc1 inhibited microglial migration whilst suppressing the inflammatory response and neuronal apoptosis by regulating the I kappa B alpha/NF-kappa B pathway, thereby improving cognitive dysfunction during SAE.

Purpose: The aim of this study was to investigate the anti-tumor effect of electroacupuncture (EA) on mice bearing breast tumors by regulating p75 neurotrophin receptor (p75NTR) and remodelling intratumoral innervation. Methods: Female BALB/c mice were implanted with 4T1 breast tumor cells to establish a murine mammary cancer model. Tumor volume and weight were measured to evaluate tumor growth. Cell apoptosis was assessed by TUNEL assay. The relative expression of p75NTR, TrkA, TrkB, NGF and proNGF were detected by immunohistochemistry. Neurotransmitter and neurotrophin were detected by enzyme-linked immunosorbent assay. Intratumoral innervation was confirmed by beta 3-tubulin and TH labeling immunohistochemistry. The antagonist TAT-Pep5 was employed to determine if the effects of EA on tumor growth and cell apoptosis were mediated by p75NTR. Results: Peritumoral EA alleviated tumor growth especially after 14 days of intervention. Apoptosis index in the tumor tissue was obviously decreased after EA. Meanwhile, EA intervention significantly upregulated the expression of p75NTR and proNGF, along with a decline in the tumor growth and an increase in the cell apoptosis. Besides, EA reduced local sympathetic innervation and downregulated sympathetic neurotransmitter NE level in the local tumor. Furthermore, p75NTR antagonist alleviated EA-mediated cell apoptosis and intratumoral innervation. Conclusions: One mechanism of EA intervention for alleviating tumor progression is mediated by p75NTR to promote apoptosis and decrease intratumoral axonogenesis in the tumor microenvironment.

化疗后血小板降低(CIT)是临床常见病,严重影响患者规范治疗.目前中医学者多从"血虚""虚劳"论治,治以温补脾肾、补气养血等方剂.我们临床观察发现,部分CIT患者辨证属于"热伏营血,毒瘀骨髓",病因与化疗药的寒热属性、患者体质、病程等因素有关.CIT因为经常引起出血应归于中医"血证"范畴而非"虚劳""血虚","血证"之病因中火邪居多,化疗药物热毒直中骨髓,热邪自内而发,向外侵及血分导致出血.治法应为"透热转气,凉血散血",组方多以"升降散""栀子豉汤""犀角地黄汤""化斑汤"等为主,并随证加减,最后附以典型医案进行论述.

Traditional Chinese herbal medicine has a long history in treating febrile diseases, according to the Shang Han Lun, a classical theory of traditional Chinese medicine (TCM) developed by Zhang Zhongjing in the Han Dynasty. Some herbs have been formulated as prescription formulae or manufactured as finished medicines such as pills, capsules, or injections. The Chinese government has recommended specific TCM prescriptions alone or combined with Western medicine to treat patients with coronavirus disease 2019 (COVID-19). Here, we introduce three prescription formulae: Qingfei Paidu decoction, Huashi Baidu formula, and Xuanfei Baidu formula; three finished medicines: Lianhua Qingwen capsules, Jinhua Qinggan granules, and Xuebijing injection; and several single herbs, such as Ephedra Herba, honeysuckle, Scutellaria, Glycyrrhizae Radix, Armeniacae Semen, Sophorae flavescentis Radix, and Curcuma longa. We review existing evidence on these traditional medicines and herbs for their related antiviral activities, efficacy, and underlying mode of action in virus-related diseases. Most of these drugs have been traditionally used in Chinese medicine for over a thousand years, and they have been proved to be safe in treating flu-like virus infections. It is necessary to further test their efficacy for treating COVID-19 and understand the underlying molecular mechanisms.

Background. We intended to explore the mechanism of Yinlai decoction in the treatment of lipopolysaccharide (LPS)-induced pneumonia from the perspective of intestinal flora. Methods. Thirty Sprague–Dawley rats were randomly assigned to the blank control group (N), the pneumonia group (P), and the Yinlai decoction group (PT). The rat pneumonia model was established using LPS inhalation (0.5 mg/mL, 5 mL, 30 min/day, 3 days). Yinlai decoction was administered intragastrically (2 mL/100 g, 3 days). Lung tissue pathology, organ indexes, serum inflammatory factors, tumor necrosis factor-alpha (TNF-α), and intestinal flora changes were measured. Results. Lung tissue inflammation was prevented by Yinlai decoction. IL-6 levels showed a higher tendency to be higher, and IL-12 and TNF-α were significantly higher in the PT group than in the P group. The structure of the intestinal flora in the P differed from that in the N. The relative abundance of 10 out of 12 microflora was significantly higher in the P group than in the N and PT groups. In the PT group, the structure and the distribution of microbial groups were like those of the N group. Conclusions. Yinlai decoction inhibited LPS-induced lung and systemic inflammation in rats and may help the intestinal flora restore equilibrium by inhibiting the colonization of pathogenic bacteria and adjusting the ratio between probiotics and pathogenic bacteria. Intestinal flora may serve as a mediator of Yinlai decoction’s effect on LPS-induced pneumonia.

甲状腺结节是临床常见病、多发病,黄金昶教授经过20余年临床实践总结,认为甲状腺结节的形成和少阳功能异常密切相关,少阳为气机升降出入的枢纽,内寄相火,是水液运行的通道.少阳枢机不利,气、火、痰、瘀壅结颈部是甲状腺结节形成的基本病机.在治疗中采用定位疏剿法治疗本病,分为一疏二调三剿;一疏为疏通局部经络郁滞,包括:刺络祛瘀疏通经络;针刺解结疏通经络;颈浅针刺横向疏通颈关;二调:左升右降通调少阳气机;三剿:结节围刺,加强针刺力量,同时结合辨证选穴治疗,临床上多获良效.

Abstract Background The outbreak of COVID-19 has resulted in serious concerns in China and abroad. To investigate clinical features of confirmed and suspected patients with COVID-19 in west China, and to examine differences between severe versus non-severe patients. Methods Patients admitted for COVID-19 between January 21 and February 11 from fifteen hospitals in Sichuan Province, China were included. Experienced clinicians trained with methods abstracted data from medical records using pre-defined, pilot-tested forms. Clinical characteristics between severe and non-severe patients were compared. Results Of the 169 patients included, 147 were laboratory-confirmed, 22 were suspected. For confirmed cases, the most common symptoms from onset to admission were cough (70·7%), fever (70·5%) and sputum (33·3%), and the most common chest CT patterns were patchy or stripes shadowing (78·0%); throughout the course of disease, 19·0% had no fever, and 12·4% had no radiologic abnormality; twelve (8·2%) received mechanical ventilation, four (2·7%) were transferred to ICU, and no death occurred. Compared to non-severe cases, severe ones were more likely to have underlying comorbidities (62·5% vs 26·2%, P = 0·001), to present with cough (92·0% vs 66·4%, P = 0·02), sputum (60·0% vs 27·9%, P = 0·004) and shortness of breath (40·0% vs 8·2%, P < 0·0001), and to have more frequent lymphopenia (79·2% vs 43·7%, P = 0·003) and eosinopenia (84·2% vs 57·0%, P = 0·046). Conclusions The symptoms of patients in west China were relatively mild, and an appreciable proportion of infected cases had no fever, warranting special attention.

目的 系统评价艾灸治疗恶性肿瘤化疗后引起的白细胞减少症的疗效.方法 通过全面检索中国知网、万方、维普、Pubmed、Wed of Science等数据库中发表的艾灸治疗化疗引起的白细胞减少症临床随机对照试验文献,用Cochorane系统评价方法,依据纳入、排除标准筛选文献、整理资料,采用Rev Man5.4软件进行质量评价和Meta分析.结果 最终纳入18篇.Meta分析显示艾灸治疗化疗后白细胞减少症较常规升白药物疗效好,差异有统计学意义.结论 艾灸治疗化疗后白细胞减少症的疗效较好,操作方便,值得推广.

目的 挖掘目前中医复方治疗三阴性乳腺癌(TNBC)的组方用药规律,分析处方相关的药物靶点及疾病通路,探索核心处方的潜在作用机制.方法 检索纳入CNKI、维普、万方、SinoMed中关于TNBC的中医临床文献,通过TCMISS软件分析组方用药规律;运用网络药理学方法获取核心处方的有效成分、治疗TNBC相关治疗靶点及靶点间相互作用网络,通过富集分析获得相关作用通路.结果 共纳入58篇文献,筛选出80首处方,挖掘出核心药物组合22个,候选新方2个,核心新处方与TNBC相关靶点共26个,其中核心靶点10个(degree≥13),相关富集通路21条,核心通路13条(P＜0.01).结论 目前中药复方对TNBC的辨治主要为疏肝健脾,消痰化瘀.其作用机制主要可能通过对肿瘤的血管生成、凋亡与增殖、炎症免疫三个方面的协同调控共同实现.

化疗后白细胞降低是临床常见病,目前中医学者多从"血虚""虚劳"论治,给予温补脾肾、补气养血等方剂.我们临床观察发现,部分化疗后白细胞降低症患者辨证并不属于"虚证"而是属于"湿热内蕴,郁遏卫阳".本文论述该证形成的病因、病机、治法、方药,其病因与化疗后脾胃损伤、运化受阻、情志不畅、郁而化火,患者火热体质,化疗药的寒热属性等三方面因素有关.其病机为白细胞与中医的"卫气"高度吻合,从"卫气"的生化及宣发来考虑湿热壅阻对于白细胞的影响.湿热壅阻中焦,导致气血生化乏源,湿热阻于上焦影响卫气宣发,共同导致白细胞降低.治法为"清利湿热,宣通卫气",组方多以"三仁汤""藿朴夏苓汤""栀子豉汤""连苏饮"等合方加减,并附以典型医案进行论述.

Background: Long non-coding RNAs (lncRNAs) play an important role in the immune processes of glioma. Immune related lncRNAs (IRlncRs) may be a critical prognosis in patients with glioma. The current study aimed to construct a glioma immune-related prognosis model by IRlncRs. Methods: Transcriptome RNA-sequencing data of glioma were obtained from The Cancer Genome Atlas (TCGA) and an immune‑related risk score (IRRS) model was constructed by Lasso and multivariate Cox regression analysis. Receiver Operating Characteristic (ROC) curves were used to assess the sensitivity and specificity of the prognosis on IRRS. A predictive nomogram and a time-dependent ROC curve was performed in training and validation cohort. We explored the relationships between survival‑related IRlncRs (sIRlncRs) and clinicopathologic parameters. Functional annotation of the sIRlncRs was investigated by gene set enrichment analysis (GSEA) and principal component analysis (PCA). The relationships between IRRS model and immune cell infiltration and co-expression network analysis among the sIRlncRs were performed for molecular mechanism study. Results: A total of 10 sIRlncRs were enrolled to build IRRS model. The IRRS was identified as an independent prognostic factor and correlated with the overall survival (AUC =0.880). The nomogram was constructed successfully with IRRS, age and grade as variables. Immune cell infiltration analysis indicated that B cells, neutrophil, dendritic and macrophage cells were positively correlated with IRRS. PCA and GSEA illustrated that the lncRNA signature enrolled the IRRS model was closely related to immune status. Additionally, co-expression network showed that there was a strong correlation between 10 sIRlncRs at the transcriptional level. Conclusion: We successfully constructed a remarkable clinical model of sIRlncRs with potential prognostic value for glioma patients, which provides an insight into immunological research and treatment strategies of glioma.