Nontuberculous mycobacteria (NTM) are of increasing public health concern. This study aimed to determine the most relevant comorbidities of NTM in Beijing, China, over a 12-year period. A retrospective analysis was performed on all 505 NTM patients diagnosed in Beijing Chest Hospital, Capital Medical University, from January 2010 to December 2021. Species identification, demographic characteristics, and comorbidities were analyzed using electronic medical records. The demographic characteristics and clinical comorbidity differences between NTM and tuberculosis (TB) patients were also analyzed. The number of patients infected with NTM in Beijing, China, has increased yearly. A total of 520 NTM were isolated from 505 inpatients, but only 465 were identified to the species level. M. intracellulare (43.44%, 202/465) and M. abscessus (128/465, 27.52%) predominated. NTM infection was associated with age, not gender. NTM infections were predominantly middle-aged (median 59 years, IQR 48.5-67) with a male-to-female ratio of 1:11. Notably, 86.1% of NTM disease had underlying conditions, most commonly malnutrition (43.0%), liver disease (31.1%), and bronchiectasis (25.0%), followed by previous TB (118/505, 23.37%), diabetes mellitus (63/505, 12.48%), hypertension (58/505, 11.49%), and pulmonary fungal infections (54/505, 10.69%). Gender-specific associations emerged: bronchiectasis was more prevalent in females (33.05% vs 17.67%, P < 0.001), while chronic obstructive pulmonary disease (COPD) predominated in males (9.77% vs 2.93%, P=0.002). Species-specific comorbidity patterns were identified: M. intracellulare was associated with malnutrition (50.50% vs 33.59%, P < 0.001) and diabetes (14.83% vs 4.69%, P < 0.001). Compared to TB, NTM cases showed stronger associations with structural lung diseases and immunosuppression. Clinical NTM infection cases increase year by year, with distinct species-specific comorbidity profiles. Our findings reveal that NTM disease is strongly associated with specific comorbidities, notably bronchiectasis, COPD, and immunological diseases. These conditions define a high-risk patient subgroup that requires targeted screening and proactive clinical management.IMPORTANCEThis study reveals a concerning rise in non-tuberculous mycobacteria (NTM) infections in Beijing, with M. intracellulare and M. abscessus as dominant species. Nearly 90% of patients had comorbidities like malnutrition, bronchiectasis, and liver disease, showing NTM's strong ties to weakened health. The work uncovers key differences from tuberculosis, including greater associations with lung damage and immunosuppression, plus gender-specific patterns (e.g., bronchiectasis in women). These findings highlight NTM as a growing threat requiring tailored diagnostic and treatment approaches, especially for vulnerable groups. The data provide crucial guidance for clinicians addressing this emerging challenge.

Nocardia species are opportunistic pathogens causing nocardiosis, often misdiagnosed as tuberculosis or nontuberculous mycobacterial infections, leading to inappropriate treatment. This study evaluates the in vitro activity of common and potential antimicrobials, including Trimethoprim-sulfamethoxazole, Amikacin, Oxazolidinones (Linezolid, Tedizolid, Contezolid), Fluoroquinolones (Moxifloxacin, Levofloxacin, Sitafloxacin), Rifampicin, and Fidaxomicin against 51 clinical Nocardia isolates. Minimum inhibitory concentrations (MICs) were determined using the AlamarBlue assay, revealing that Linezolid exhibited significant efficacy against all isolates, while Trimethoprim-sulfamethoxazole and Amikacin showed 92.16% sensitivity. Sitafloxacin demonstrated superior efficacy among Fluoroquinolones, with variations across Nocardia species. Fidaxomicin exhibited significant activity (88.24%), contrasting with Rifampicin's limited effect. A high prevalence of the gyrA Ser83Ala mutation was identified in resistant Nocardia strains, correlating with reduced Fluoroquinolone susceptibility. These findings highlight the need for tailored treatment strategies based on species-specific susceptibility and resistance profiles and suggest Fidaxomicin and Sitafloxacin as promising options. Further clinical validation is warranted to optimize therapeutic outcomes.

BACKGROUND:Currently, the mechanisms by which otitis media with effusion (OME) progresses to intractable OME is unclear. Since crosstalk between microbiome and host contributes to many diseases, we hypothesized that similar interactions could occur in the middle ear effusion (MEE) samples from patients with OME and influence intractable OME pathogenesis. This study aimed to evaluate the microbial profile of MEE samples and to determine whether there were microbial differences between the MEE microbiota of patients with intractable OME and those with rapidly cured OME. METHODS:MEE samples were collected from 46 OME patients, including 20 from the long course group and 26 from the short course group. Metagenomic sequencing was performed on 30 of these samples, allowing the identification of microbial differences associated with varying disease durations. The difference was verified by further experimental validation, including fluorescence in situ hybridization (FISH) and quantitative polymerase chain reaction (qPCR). RESULTS:The alpha diversity indices and overall MEE microbial structure show no significant difference between the long course and short course groups, but species such as Bacillus cereus, Nocardiopsis dassonvillei, and Rothia aeria are significantly more prevalent in the MEE of long course OME patients. qPCR analyses and FISH also confirm the difference in the abundance of Bacillus cereus between the two groups. CONCLUSIONS:Bacillus cereus plays a role in the persistence of OME infection and serves as a potential biomarker to predict OME prognosis. Further studies are warranted to explore the value of Bacillus cereus detection in informing early intervention.

Background:Lung cancer remains a leading cause of cancer-related mortality, with poor survival outcomes. Despite the widespread use of programmed cell death protein 1 (PD-1) blockade therapy, more than 70% of patients fail to benefit and might even develop adverse inflammatory responses. Clinical observations have shown that patients with high neutrophil levels experience worse outcomes following PD-1 blockade. However, the underlying mechanism remains elusive. This study aimed to investigate the impact of neutrophils on anti-PD-1 therapy in lung cancer. Methods:Clinical cohort analysis revealed that peripheral neutrophil levels correlated with survival and metastasis in non-small cell lung cancer (NSCLC) patients treated with PD-1 blockade. In this study, we established a subcutaneous Lewis lung carcinoma (LLC) mouse model, and depleted neutrophils by anti-Ly6G antibody with or without PD-1 blockade. Dynamic changes of peripheral immune cells (CD4+T cells, CD8+ T cells, macrophages, neutrophils, and myeloid-derived cells) in mice were examined by Flow cytometry during treatment, and cytokine levels were measured using Luminex multiplex assays. Results:Clinically, patients with high neutrophil counts exhibited significantly shorter progression-free survival (PFS) and overall survival (OS), and were more prone to distant organ metastases. In the mouse model, neutrophil depletion enhanced CD8+ T cell infiltration in tumor tissues and suppressed neutrophil-mediated interleukin (IL)-5, IL-6 and IL-17A inflammation, resulting in the inhibition of tumor growth. However, the combination of neutrophil depletion with PD-1 blockade paradoxically restored inflammatory cytokine production and increased myeloid-derived suppressor cell (MDSCs) infiltration, thereby compromising tumor suppression. Conclusions:Our observation shows that high neutrophil levels in cancer patients are associated with poorer prognosis and increased risk of distant metastasis. Depletion of neutrophils reshapes the tumor immune microenvironment, wherein excessive inflammatory cytokines drive resistance to PD-1 antibody therapy.

Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant disorder with variable manifestations, including recurrent epistaxis, telangiectasias, arteriovenous malformations, and family history. It is caused by heterozygous null alleles of ENG , ACVRL1 , SMAD4 , or BMP9 , with delayed clinical diagnosis. Genetic testing is crucial for early diagnosis. To analyze the variant distribution of HHT-related genes, expand variant databases for Chinese patients, and explore phenotype-genotype associations. Thirty-two individuals from 20 unrelated families were recruited. Coding regions of ENG , ACVRL1 , SMAD4 , and BMP9 were sequenced. Variants were identified by sequence alignment. Epistaxis severity was evaluated using the epistaxis severity score (ESS), and the ESS differences between groups were analyzed using the Mann–Whitney test. Seventeen unique variants were identified in 17 unrelated HHT families (17/20, 85%), including 5 novel variants (3 in ENG and 2 in ACVRL1 ). Eleven ACVRL1 variants were identified in 12 families (12/17, 70.6%). Six variants of ENG were detected in 5 families (5/17, 29.4%), and one patient had two variants. ACVRL1 variants were 2.4 times more prevalent than ENG variants, with 41.7% of ACVRL1 variants in exon 10. A recurrent variant, c.1435C>T, was identified in two families. Epistaxis severity increased with age. ACVRL1 variants were more common than ENG variants in Chinese HHT families, with exon 10 identified as a potential hotspot. These findings enhance understanding of HHT genetics and guide targeted genetic testing in China.

The aim of this study was to reveal diagnostic biomarkers of considerable importance for common pathogenic Nocardia, utilizing pan-genomic and comparative genome analysis to accurately characterize clinical Nocardia infections. In this study, complete or assembled genome sequences of common pathogenic Nocardia and closely related species were obtained from NCBI as discovery and validation sets, respectively. Genome annotation was performed using Prokka software, and pan-genomic analysis and extraction of Nocardia core genes were performed using BPGA software. Comparative genome analysis of these core genes with the validation-set gene sequences was then performed using BLAT, with a threshold of 30% amino acid coverage and identity, in order to distinguish specific core genes. Finally, candidate gene-specific primers were designed using Snapgene software and DNA samples were obtained from clinical Nocardia strains and closely related species for validation. The analysis identified eighteen core genes specific to Nocardia spp., four core genes specific to N. farcinica, and forty-six core genes specific to N. cyriacigeorgica. After rigorous clinical validation, one gene from Nocardia spp. and five genes from N. cyriacigeorgica were confirmed to have high specificity and therefore can be used as reliable biomarkers for accurate diagnosis of Nocardia infection. This pioneering research reveals diagnostic biomarkers of considerable significance, with the potential to substantially enhance the precise diagnosis of common pathogenic Nocardia infections, thereby laying the groundwork for innovative diagnostic methodologies in subsequent studies.

The immune characteristics and pathological mechanisms of COVID-19 and tuberculosis coinfection are not well understood. Single-cell RNA sequencing has emerged as a powerful tool for dissecting complex immune responses and cellular interactions in infectious diseases. Here, we employed scRNA-seq, combined with laboratory examinations and clinical observations, to elucidate potential mechanisms of immunopathology and protective immunity in coinfected patients. Substantial alterations in immune cell populations in patients with severe coinfection were observed, characterized by severe lymphopenia and massive expansion of myeloid cells. Lymphocytopenia may have resulted from lymphocyte apoptosis and migration. Systemic upregulation of S100 family proteins, mainly released by classical monocytes, might contribute to inflammatory cytokine storm via S100-TLR4-MyD88 signaling pathway in severely coinfected patients. Myeloid cells may contribute to immune paralysis in severe cases through expansion of myeloid-derived suppressor cells and dysregulated dendritic cell function. The immune landscape of T cells in severe patients were featured by dysregulated Th1 response, widespread exhaustion and increased cytotoxic, apoptosis, migration and inflammatory states. We observed increased plasma cells and overexpression of B-cell-activation-related pathways in severe patients. Together, we provide a comprehensive atlas illustrating the immune response to coinfected patients at the single-cell resolution and highlight mechanisms of pathogenesis in severe patients.

Background: Coronavirus disease 2019 (COVID-19) and tuberculosis (TB) co-infection (COVID-19-TB) has the potential to exacerbate lung damage; however, information about the clinical features of COVID-19-TB is limited. This study aims to clarify the clinical characteristics and outcomes of patients with COVID-19-TB. Methods: In this single-center retrospective study, the clinical features and outcomes of patients with COVID-19 with active TB who were admitted to Beijing Chest Hospital, Beijing, China, from 1 December 2022 to 18 January 2023 were collected. The severity of COVID-19 and TB was graded according to guidelines from the World Health Organization. The relationships of demographic and clinical variables with intensive care unit (ICU) admission were evaluated using univariable and multivariable logistic regression models. Results: Overall, 102 patients with COVID-19-TB were enrolled. The mean age was 54.5 years (range 36.5–70 years). The most common clinical manifestations were cough (68.63%), sputum production (53.92%), fever (51.96%), and ground-glass opacities (35.29%). Complications included acute respiratory distress syndrome (11.76%), sepsis (9.8%), and respiratory failure (7.84%). Patients with COVID-19-TB had high concentrations of various proinflammatory cytokines, including interferon-γ, interleukin-1β, interferon-γ-inducible protein 10 kD, and monocyte chemoattractant protein-1. Sixteen of the 102 patients with COVID-19-TB (15.69%) were admitted to the ICU, and 10 (9.80%) died during hospitalization. The significant risk factors for ICU admission were respiratory failure, pulmonary fungal infection, and ventilation and oxygen therapy. Conclusions: The mortality rate of COVID-19-TB was 9.80%. Several demographic and clinical characteristics were associated with adverse outcomes, indicating the importance of early recognition and treatment.

Cancer immunotherapy such as immune checkpoint blockade (ICB) therapy has made important breakthroughs in cancer treatment, however, currently only parts of cancer patients benefit from ICB therapy. The suppressive tumor immune microenvironment (TIME) impedes the treatment response of immunotherapy, indicating the necessity to explore new treatment targets. Here, we reported a new potential immunotherapeutic target, Dickkopf-3 (DKK3), for cancer treatment. DKK3 expression is up-regulated in the tumors from multiple cancer types, and high DKK3 expression is associated with worse survival outcome across different cancers. We observed that DKK3 directly inhibits the activation of CD8+ T cells and the Th1 differentiation of CD4+ T cells ex vivo. Also, by establishing four different mouse cancer models, we found that DKK3 blockade triggers effective anti-tumor effects and improve the survival of tumor-bearing mice in vivo. DKK3 blockade also remodels the suppressive TIME of different cancer types, including the increased infiltration of CD8+ T cells, IFN-γ+CD8+ T cells, Th1 cells, and decreased infiltration of M2 macrophages and MDSCs in the TIME. Moreover, we found that combined blockade of DKK3 and PD-1 induces synergistic tumor-control effect in our mouse cancer model. Therefore, our study reveals the impact of DKK3 in the TIME and cancer progression, which suggests that DKK3 is a novel and promising immunotherapeutic target for enhanced cancer immunotherapy.

Introduction:Diagnosing tuberculosis (TB) in HIV-infected individuals presents significant challenges due to difficulties in obtaining specimens containing adequate quantities of Mycobacterium tuberculosis (Mtb). This study aimed to evaluate the diagnostic performance of the IP-10 mRNA assay independently and in combination with established diagnostic tests for Mtb detection. Methods:The study cohort comprised 111 HIV-infected individuals who presented with TB at Beijing Youan Hospital from 2022 to 2024. Participants were categorized into confirmed TB, probable TB, or non-TB groups according to the diagnostic criteria for tuberculosis (WS288-2017). The performance of the IP-10 mRNA release assay was evaluated by the STARD guidelines on blood samples collected after enrollment. Results:The IP-10 mRNA release assay demonstrated significantly higher sensitivity than interferon-γ release assays (IGRAs) and culture methods for confirming pulmonary tuberculosis (PTB) diagnosis while maintaining comparable specificity. Receiver operating characteristic (ROC) analysis revealed that the diagnostic performance of the IP-10 mRNA release assay used in parallel with Xpert MTB/RIF significantly exceeded that of the IP-10 mRNA release assay alone (0.731 vs. 0.687, P=0.02). Among HIV-infected individuals, the IP-10 mRNA release assay showed superior performance compared to IGRAs for diagnosing extrapulmonary tuberculosis. Conclusions:The IP-10 mRNA release assay exhibited excellent diagnostic performance and demonstrates substantial potential as an auxiliary tool for diagnosing TB in HIV-infected individuals. The combined application of IP-10.TB and Xpert MTB/RIF further enhance diagnostic efficacy.

Thyroid cancer (THCA) shows rising incidence and aggressiveness in young-onset cases. Through integrated single-cell, transcriptomic, and proteomic analyses, we identified age-specific tumor-associated macrophage (TAM) genes, including OLR1 and SIGLEC1, linked to metastasis and immune dysfunction. These TAM biomarkers were validated at the protein level, highlighting their prognostic and therapeutic potential. Our findings reveal key TAM-driven mechanisms in young-onset THCA progression, warranting further clinical investigation.

Background: Immune checkpoint inhibitors (ICIs) hold a great promise in treatment of non-small cell lung cancer (NSCLC), while only a portion of patients benefited from the treatment, and others could not achieve optimal therapeutic effects from initial immunotherapy, even for those patients with PD-L1 (Programed cell death ligand 1) tested positive. However, the clinical markers for the selection of patients who will benefit from ICIs combination treatment beforehand are largely unknown. Objectives: The purpose of this study was to explore the non-invasive biomarkers that can predict the efficacy of immune combination therapy in advanced/metastatic NSCLC patients. Design: This study employed a retrospective cohort design to analyze dual predictive biomarkers in advanced non-small cell lung cancer (NSCLC) patients with immune combination therapy. Method: An analysis was conducted on baseline information of 144 patients with advanced/metastatic NSCLC who received ICIs treatment from the November of 2018 to the January of 2023 in Beijing Chest Hospital. We established a scoring group chart to make quantitative prediction for overall survival (OS) and progression-free survival (PFS) based on 4 variables, and set up the nomogram model as well as Decision curve analysis (DCA) to assess clinical benefits of ICIs combination in treatment of patients with advanced/metastatic NSCLC. Results: We found that serum globulin (GLB) >26.6 (g/L) (HR = 1.865, P = .002), absolute neutrophil counts (ANC) (10 9 /L) > 5 (HR = 2.146, P < .001), and bone metastasis (HR = 2.148, P < .001) were independent factors affecting the PFS of NSCLC patients. GLB > 26.6 (g/L) (HR = 1.741, P = .018), ANC (10 9 /L) >5 (HR = 1.807, P = .008), bone metastasis (HR = 1.651, P = .002), and PD-L1 Negative (HR = 2.432, P = .032) were independent factors affecting the OS of NSCLC patients. Same variables and cut-off value have good predictive efficacy in both PFS and OS. Conclusion: In patients with advanced/metastatic NSCLC receiving ICIs combination treatment, the GLB, ANC, bone metastasis, and PD-L1 may serve as useful predictive markers for the prognosis of NSCLC patients with ICIs combination treatment.

Menopause is characterized by the cessation of menstruation and a decline in reproductive function,which is an intrinsic component of the aging process.However,it has been a frequently overlooked field of women's health.The oral and gut microbiota,constituting the largest ecosystem within the human body,are important for maintaining human health and notably contribute to the healthy aging of menopausal women.Therefore,a comprehensive review elucidating the impact of the gut and oral microbiota on menopause for healthy aging is of paramount importance.This paper presents the current understanding of the microbiome during menopause,with a particular focus on alterations in the oral and gut microbiota.Our study elucidates the complex interplay between the microbiome and sex hormone levels,explores mi-crobial crosstalk dynamics,and investigates the associations between the microbiome and diseases linked to menopause.Additionally,this review explores the potential of microbiome-targeting therapies for managing menopause-related diseases.Given that menopause can last for approximately 30 years,gaining insights into how the microbiome and menopause interact could pave the way for innovative interventions,which may result in symptomatic relief from menopause and an increase in quality of life in women.

Abstract Background Maternal overweight/obesity and excessive gestational weight gain (GWG) are frequently reported to be risk factors for obesity and other metabolic disorders in offspring. Cord blood metabolites provide information on fetal nutritional and metabolic health and could provide an early window of detection of potential health issues among newborns. The aim of the study was to explore the impact of maternal prepregnancy overweight/obesity and excessive GWG on cord blood metabolic profiles. Methods A case control study including 33 pairs of mothers with prepregnancy overweight/obesity and their neonates, 30 pairs of mothers with excessive GWG and their neonates, and 32 control mother-neonate pairs. Untargeted metabolomic profiling of umbilical cord blood samples were performed using UHPLC‒MS/MS. Results Forty-six metabolites exhibited a significant increase and 60 metabolites exhibited a significant reduction in umbilical cord blood from overweight and obese mothers compared with mothers with normal body weight. Steroid hormone biosynthesis and neuroactive ligand‒receptor interactions were the two top-ranking pathways enriched with these metabolites (P = 0.01 and 0.03, respectively). Compared with mothers with normal GWG, in mothers with excessive GWG, the levels of 63 metabolites were increased and those of 46 metabolites were decreased in umbilical cord blood. Biosynthesis of unsaturated fatty acids was the most altered pathway enriched with these metabolites (P < 0.01). Conclusions Prepregnancy overweight and obesity affected the fetal steroid hormone biosynthesis pathway, while excessive GWG affected fetal fatty acid metabolism. This emphasizes the importance of preconception weight loss and maintaining an appropriate GWG, which are beneficial for the long-term metabolic health of offspring.

Abstract Purpose This study aims to utilize pan-genome and comparative genome analysis techniques to reveal diagnostic biomarkers of considerable importance for common pathogenic Nocardia, thereby facilitating accurate identification of clinical Nocardia infections. Methods Complete or assembled genome sequences of common pathogenic Nocardia and closely related species were obtained from NCBI (https://www.ncbi.nlm.nih.gov/) as discovery and validation sets, respectively. Genome annotation was performed using Prokka software, and pan-genomic analysis and extraction of Nocardia core genes were performed using BPGA software. Comparative genome analysis of these core genes with the validation set gene sequences was then performed using BLAT, with a threshold of 30% amino acid coverage and identity to distinguish specific core genes. Finally, candidate gene-specific primers were designed using Snapgene software and DNA samples were obtained from clinical Nocardia strains and closely related species for validation. Results The analysis identified 18 core genes specific to Nocardia spp., 4 core genes specific to N. farcinica, and 46 core genes specific to N. cyriacigeorgica. After rigorous clinical validation, 1 gene (F6W96_34950) from Nocardia spp. and 5 genes (NCTC10797_02287, NCTC10797_01760, NCTC10797_05842, NOCYR_2299 and C5B73_13220) from N. cyriacigeorgica all showed relatively high specificity, suggesting their potential as promising biomarkers for the diagnosis of Nocardia infections. Conclusion This pioneering research reveals diagnostic biomarkers of considerable significance, with the potential to substantially enhance the precise diagnosis of common pathogenic Nocardia infections, thereby laying the groundwork for innovative diagnostic methodologies in subsequent studies.

Introduction: Chronic obstructive pulmonary disease (COPD) is a prevalent condition worldwide, and standardized targeted treatments can effectively control its symptoms. However, the efficacy of the Bufei formula or its modified versions as an adjuvant treatment for preventing COPD exacerbations has not been well established. Methods: To evaluate the effectiveness of the Bufei and modified Bufei formulas, a systematic review followed by a meta-analysis was conducted. In September 2024, four databases were searched for randomized controlled trials investigating the use of the Bufei formula and its variations in treating COPD. Results: Four studies were included in this meta-analysis: one on the Bufei formula and three on the Bufei Yishen formula, encompassing 775 patients. The Bufei and Bufei Yishen formulas demonstrated effectiveness in preventing COPD exacerbations, with mean differences (MD) of −0.6 times/person-year (95% CI: −0.68 to −0.52, p < 0.001) and −0.39 (95% CI: −0.47 to −0.32, p < 0.001; I2 = 0%), respectively. The combined effect of both formulas in reducing exacerbations was −0.45 (95% CI: −0.60 to −0.31, p < 0.001; I2 = 77%). For reducing dyspnea as measured by the modified Medical Research Council dyspnea scale, the Bufei and Bufei Yishen formulas showed mean differences of -0.39 points (95% CI: −0.62 to −0.16, p < 0.001) and −0.46 points (95% CI: −0.67 to −0.26, p < 0.001; I2 = 48%), respectively. Additionally, two studies evaluated the Bufei Yishen formula’s effectiveness in improving the 6-minute walking distance, showing a mean difference of 37.0 meters (95% CI: 21.1 to 52.9, p < 0.001; I2 = 0%). Conclusion: Bufei and Bufei Yishen formulas are effective adjuvant treatments for COPD.

Head and neck squamous cell carcinoma (HNSCC) is one of the most heavily immune infiltrated human tumors, having distinct immune subtypes associated with different molecular characteristics and clinical outcomes. The tumor microenvironment (TME) of HNSCC which was dominated by tumor-associated macrophages (TAMs) had a relatively inferior prognosis. High levels of oxidized low-density lipoprotein receptor 1 (OLR1) expression are associated with more aggressive and metastatic characteristics in multiple cancers. However, the link between the OLR1 expression and immunosuppression of TME, and the molecular mechanisms which govern intratumoral TAMs behavior are unclear. Here, we performed the transcriptional analysis based on a single-cell RNA-sequencing (scRNA-seq) dataset of HNSCC, and found that the OLR1 expression was specifically enriched on the TAMs. Evaluation of protein expression within histologic sections of primary HNSCC patient samples showed a co-expression pattern of OLR1 and CD68 on macrophages. A total of 498 tumor samples of HNSCC patients from The Cancer Genome Atlas (TCGA) database were also analyzed. Remarkably, OLR1 expression was dramatically higher in HNSCC tissues than that in adjacent normal tissues, and the patients with high levels of OLR1 expression had significantly unfavorable overall survival (Hazard Ratio = 1.724, log-rank P-value = 0.0066) when compared to patients harboring low expression levels of OLR1. In summary, we reported that the specific expression of OLR1 on the TAMs was significantly correlated with poor survival outcomes, revealing that OLR1 could serve as a potential prognosis marker and promising target for immunotherapy in HNSCC.