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At least 19 recordsLinked to original sources
PubMed1978

Deficient cell-mediated immunity in head and neck cancer patients secondary to autologous suppressive immune cells.

Fifty-four patients with epidermoid head and neck cancer were studied with routine and modified mixed leukocyte culture (MLC) techniques to quantify and characterize their cell-mediated immunity (CMI). Of these, 67% demonstrated deficient CMI in MLC. Employing G-10 column filtration to remove adherent cells selectively, the authors found that 56% of these deficient individuals demonstrated significantly increased lymphocyte responsiveness in MLC. Returning the adherent cells to the cultures usually recaptured the suppressive effect of these adherent cells. Cell marker analyses reveal that the macrophage is the most likely candidate for this suppressive cell. Therapeutic measures which address this paradoxically suppressive cell could be of benefit in enhancing CMI and gaining tumor control.

Carcinoma, Squamous Cell↗
PubMed1975

Nucleoside-phosphorylase deficiency in a child with severely defective T-cell immunity and normal B-cell immunity.

A 5-year-old girl with a history of recurrent infection and anaemia has no measurable purine nucleoside phosphorylase (N.P.) activity in her red blood-cells. Her serum-immunoglobulin levels are normal, as are her antibody responses to thymus dependent and independent antigens. However, she has severe lymphopenia, pronounced depression of lymphocyte response to mitogenic and allogeneic cell stimuli, and greatly decreased T-cell rosette formation. Her parents are second cousins; their red cells contain less than half the normal level of N.P. activity. They also share an unusual N.P. isozyme pattern indicative of molecular hybridisation between catalytically active and inactive subunits, which strongly supports the assumption that they are heterozygous and their daughter is homozygous for a "silent" allele at the N.P. gene locus. Inherited deficiency of adenosine deaminase, an enzyme catalysing a reaction only one metabolic step away from that of N.P., is known to cause immunodeficiency. It is therefore very likely that this patient's lack of demonstrable N.P. activity is responsible for her syndrome.

B-Lymphocytes↗
PubMed1976

DNA synthesis in vitro by cells from mice immunized with picryl chloride: effect of injection of immune cells.

Mice were immunized with picryl chloride and the regional nodes taken at various times afterwards. These cells spontanesouly synthesized DNA in vitro as measured by thymidine incorporation over an 18-hour period and the peak incorporation occurred when the cells were takin on day 3. When the mice were injected with cells taken 5 days after immunization with picryl chloride and then immunized, there was a depression of the spontaneous DNA synthesis in vitro. This was absent on day 2, most marked on day 3 and still present on day 4. Cells from donors immunized with 4-ethoxymethylene-2-phenyloxazolone had a smaller but definite effect. Attempts to reproduce the phenomenon by in vitro mixtures of cells taken at various times after immunization in vivo were unsuccessful.

Animals↗
PubMed2026

In vivo immune cell engineering from bench to clinical reality.

Adoptive immune cell therapies, exemplified by chimeric antigen receptor T cells, have transformed the treatment of hematological malignancies. However, their broader clinical application is limited by complex ex vivo manufacturing, high cost, and safety concerns. In vivo immune cell engineering has emerged as an alternative strategy that delivers genetic instructions directly to immune cells, thereby generating or modulating therapeutic immune cells within the body and reducing the reliance on individualized in vitro operations. These advances underscore the need for a systematic evaluation of this emerging field. Therefore, this review systematically summarizes the mechanistic principles and delivery strategies underlying in vivo immune cell engineering, with an emphasis on in vivo CAR-T cell generation and the engineering of other immune cells. We then discuss major viral and non-viral delivery platforms and clarify how these platforms influence cargo delivery, cell specificity, and functional immune-cell programming. We further discuss recent preclinical and emerging clinical advances across cancer, autoimmune diseases, and degenerative diseases, while examining key translational challenges, including delivery specificity, off-target effects, controllability, persistence, and manufacturing standardization. Overall, although the field of in vivo immune cell engineering is advancing rapidly, its clinical success will depend on coordinated improvements in delivery precision, therapeutic efficacy, safety, and controllable immune-cell programming.

Cancer immunotherapy↗
PubMed2025

Tumor-immune partitioning and clustering algorithm for identifying tumor-immune cell spatial interaction signatures within the tumor microenvironment.

BACKGROUND: Growing evidence supports the importance of characterizing the organizational patterns of various cellular constituents in the tumor microenvironment in precision oncology. Most existing data on immune cell infiltrates in tumors, which are based on immune cell counts or nearest neighbor-type analyses, have failed to fully capture the cellular organization and heterogeneity. METHODS: We introduce a computational algorithm, termed Tumor-Immune Partitioning and Clustering (TIPC), that jointly measures immune cell partitioning between tumor epithelial and stromal areas and immune cell clustering versus dispersion. As proof-of-principle, we applied TIPC to a prospective cohort incident tumor biobank containing 931 colorectal carcinoma cases. TIPC identified tumor subtypes with unique spatial patterns between tumor cells and T lymphocytes linked to certain molecular pathologic and prognostic features. T lymphocyte identification and phenotyping were achieved using multiplexed (multispectral) immunofluorescence. In a separate hepatocellular carcinoma cohort, we replaced the stromal component with specific immune cell types-CXCR3+CD68+ or CD8+-to profile their spatial relationships with CXCL9+CD68+ cells. RESULTS: Six unsupervised TIPC subtypes based on T lymphocyte distribution patterns were identified, comprising two cold and four hot subtypes. Three of the four hot subtypes were associated with significantly longer colorectal cancer (CRC)-specific survival compared to a reference cold subtype. Our analysis showed that variations in T-cell densities among the TIPC subtypes did not strictly correlate with prognostic benefits, underscoring the prognostic significance of immune cell spatial patterns. Additionally, TIPC revealed two spatially distinct and cell density-specific subtypes among microsatellite instability-high colorectal cancers, indicating its potential to upgrade tumor subtyping. TIPC was also applied to additional immune cell types, eosinophils and neutrophils, identified using morphology and supervised machine learning; here two tumor subtypes with similarly low densities, namely 'cold, tumor-rich' and 'cold, stroma-rich', exhibited differential prognostic associations. Lastly, we validated our methods and results using The Cancer Genome Atlas colon and rectal adenocarcinoma data (n = 570). Moreover, applying TIPC to hepatocellular carcinoma cases (n = 27) highlighted critical cell interactions like CXCL9-CXCR3 and CXCL9-CD8. CONCLUSIONS: Unsupervised discoveries of microgeometric tissue organizational patterns and novel tumor subtypes using the TIPC algorithm can deepen our understanding of the tumor immune microenvironment and likely inform precision cancer immunotherapy.

Humans↗
PubMed2026

Deciphering miRNA-mediated genetic architecture of immune cell subsets in hypertrophic scars and keloids: A 2-step Mendelian randomization study unveiling causal associations.

This study aimed to investigate the potential causal roles of specific circulating microRNAs (miRNAs) and immune cell subsets in the pathogenesis of hypertrophic scars and keloids using a 2-step Mendelian randomization framework. We employed a 2-sample Mendelian randomization approach to evaluate the causal relationships between miRNAs, immune cell genotypes, and scar phenotypes. The analysis integrated miRNA expression quantitative trait loci, immune cell genome-wide association studies, and scar datasets. A 2-step mediation analysis was conducted to assess the indirect effects of miRNAs on scars through immune cell genotypes, using inverse variance weighted methods and complementary sensitivity analyses to ensure robustness. Our analysis identified significant associations between specific miRNAs and scar phenotypes. Notably, miR-6887-5p exhibited a total effect on keloid formation risk (β = 0.324, 95% confidence interval [CI]: 0.073-0.576) and a direct effect (β = 0.283, 95% CI: 0.027, 0.538), with a marginally significant mediation effect through B-cell activating factor receptor on CD20- CD38- B cells (β = 0.042, 95% CI: -0.001, 0.084, P = .047). For hypertrophic scars, miR-345-5p demonstrated a significant total effect (β = -0.501, 95% CI: -0.903, -0.099) and direct effect (β = -0.469, 95% CI: -0.872, -0.066), with a significant mediation effect through CD28+ CD45RA- CD8dim T cell percentage (β = -0.032, 95% CI: -0.062, -0.002, P = .034). miR-4801 showed a significant total effect (β = -0.246, 95% CI: -0.429, -0.064) and direct effect (β = -0.218, 95% CI: -0.402, -0.033), with a marginally significant mediation effect through T cell absolute count (β = -0.028, 95% CI: -0.057, -0.000, P = .043). These findings highlight the interplay between miRNAs and immune cell subsets in scar pathogenesis. This study provides preliminary evidence for the causal roles of specific miRNAs and immune cell subsets in scar formation, emphasizing the potential of miRNA-immune cell axes as therapeutic targets. While the identified associations offer important insights into the molecular mechanisms of scar heterogeneity, further validation through mechanistic studies and clinical trials is necessary to translate these genetic insights into clinical interventions.

Humans↗
PubMed2026

Novel Insights into Immune Cell Function in Type 2 Diabetes Mediated by Gut Microbiota: A Two-Sample Mendelian Randomization Study.

INTRODUCTION: The role of immune cells in type 2 diabetes mellitus (T2DM) development is well-studied, but their interactions with the gut microbiota and the mediating role in this process remain unclear. METHODS: We analyzed 731 immune cell phenotypes (3,757 Europeans), 473 gut microbiota traits (5,959 Finns), and T2DM data (over 400,000 Finns). Mendelian randomization (MR) was based on three assumptions: the instrumental variable (IV) is associated with exposure, IV is not influenced by confounding, and IV affects the outcome only through exposure. We selected single-nucleotide polymorphisms (SNPs) from genome-wide association studies as instrumental variables (IVs) to infer causal effects in two-sample MR analysis. RESULTS: We identified 36 immune cell phenotypes associated with T2DM, including 29 protective factors and seven risk factors, as well as 10 gut microbiota significantly linked to T2DM, with eight protective factors and two risk factors. MR revealed that five gut microbiota mediated the relationship between immune cells and T2DM. For example, the effects of CD3 on resting Treg (OR: 1.0136), CD3 on CM CD4+ (OR: 1.0180), and CD3 on naive CD4+ cells (OR: 1.0150) in T2DM were found to be partially mediated by the species Bacillus. AYThe corresponding mediation effect proportions were 8.99%, 11.8%, and 11.4%. DISCUSSION: MR analysis identified multiple gut microbiota mediators in the relationship between immune cells and T2DM, addressing previous observational evidence. Limitations included the European ancestry bias, among others. CONCLUSION: This study has highlighted the gut microbiota as a mediator between immune cells and T2DM, offering new insights for its early prevention and intervention.

Diabetes Mellitus, Type 2↗
PubMed2026

Plasma lipid species, immune cell traits, and gastric cancer risk: A Mendelian randomization study.

Plasma lipid composition has been linked to multiple cancers, yet its causal contribution to gastric cancer and the potential intermediary role of immune cells remain unclear. We aimed to clarify these relationships and identify specific lipid and immune cell traits that either protect against or promote gastric cancer. We performed a 2-sample, 2-step Mendelian randomization analysis using summary statistics from large genome-wide association studies of gastric cancer (1423 cases, 3,14,193 controls), plasma lipidomics (179 molecular species), and 731 immune cell phenotypes. Independent, genome-wide significant single-nucleotide variants served as instrumental variables. First, we estimated the causal effects of each plasma lipid on gastric cancer. Then, we explored the potential intermediary role of lipid-associated immune cell traits using a 2-step Mendelian randomization framework. Two lipids - phosphatidylethanolamine (18:0 0:0) and phosphatidylcholine (O-18:0 16:1) - were causally associated with a lower risk of gastric cancer. Three immune cell traits (CD8br and CD8dim %leukocyte, IgD on IgD+ CD38- and CD3 on CD28- CD8br) similarly showed protective effects. In contrast, phosphatidylcholine (O-16:1 18:2), triacylglycerol (49:1), triacylglycerol (56:3), and triacylglycerol (56:4) increased gastric cancer risk, as did immune traits such as TD DN (CD4-CD8-)AC, CD19 on memory B cell, CD28 on CD39+ activated Treg, CD45 on CD4+, CD127 on CD28+DN(CD4-CD8-) and CCR2 on CD14+CD16+ monocyte. Exploratory mediation analyses found no statistically significant evidence that immune cell traits mediated the effects of plasma lipids on gastric cancer risk. Specific phosphatidylethanolamines and phosphatidylcholines confer protection against gastric cancer, whereas several triacylglycerols increase risk. However, exploratory mediation analyses provided no statistically significant evidence that immune cell traits mediated these associations.

Humans↗
PubMed2024

Exploring correlations between immune cell phenotypes and the risk of epilepsy: A bidirectional Mendelian randomization study.

BACKGROUND: Neuroinflammation plays an important pathophysiological role in epilepsy; however, the precise connection between immune cells and epilepsy remains unclear. This study used Mendelian randomization (MR) to analyze the causal relationship between 731 immune cell traits and epilepsy. METHODS: Based on data from a genome-wide association study (GWAS), a bidirectional two-sample MR analysis was conducted to investigate the potential influence of immune cell phenotypes on epilepsy. Five MR methods were used to analyze the results, with the inverse variance weighted (IVW) method as the primary method, and the results were corrected using the false discovery rate (FDR) method. Sensitivity analyses were performed to test for heterogeneity and horizontal pleiotropy. RESULTS: After correction for FDR, four immune traits remained significantly associated with epilepsy risk: CD25 expression on memory (OR = 1.04, 95 % CI = 1.02 ∼ 1.06,P = 2.55 × 10-4), IgD+CD38dim (OR = 1.05, 95 % CI = 1.02 ∼ 1.08, P = 4.73 × 10-4), CD24+CD27+ (OR = 1.04, 95 % CI = 1.02 ∼ 1.06, P = 4.82 × 10-4), and IgD-CD38dim (OR = 1.04, 95 % CI = 1.02 ∼ 1.06, P = 1.04 × 10-3) B cells. The risk of generalized epilepsy was significantly associated with two immune cell traits, whereas that of focal epilepsy was significantly associated with seven immune cell traits. Furthermore, immune cell phenotypes are not affected by genetically predicted epilepsy. CONCLUSION: This MR study affirms the causal connection between circulating immune cells and epilepsy, offering guidance for further understanding of the immune mechanisms that underlie epilepsy and the discovery of novel targets for therapy.

Humans↗
PubMed2025

Multimodal profiling reveals tissue-directed signatures of human immune cells altered with age.

The immune system comprises multiple cell lineages and subsets maintained in tissues throughout the lifespan, with unknown effects of tissue and age on immune cell function. Here we comprehensively profiled RNA and surface protein expression of over 1.25 million immune cells from blood and lymphoid and mucosal tissues from 24 organ donors aged 20-75 years. We annotated major lineages (T cells, B cells, innate lymphoid cells and myeloid cells) and corresponding subsets using a multimodal classifier and probabilistic modeling for comparison across tissue sites and age. We identified dominant site-specific effects on immune cell composition and function across lineages; age-associated effects were manifested by site and lineage for macrophages in mucosal sites, B cells in lymphoid organs, and circulating T cells and natural killer cells across blood and tissues. Our results reveal tissue-specific signatures of immune homeostasis throughout the body, from which to define immune pathologies across the human lifespan.

Humans↗
PubMed1978

Immunological studies of T-cell receptors. I. Specifically induced resistance to graft-versus-host disease in rats mediated by host T-cell immunity to alloreactive parental T cells.

The present studies extend our previous efforts to understand the immunological basis of specifically induced graft-versus-host (GVH) resistance in F1 hybrid rats. Immunization of F1 rats with alloreactive T-cell populations of parental strain origin induces a host-mediated T-cell response which is specific for anti-major hostocompatibility complex receptors on parental T cells. This protective immunity is rapid in onset and once induced, it provides a highly effective, specific resistance to lethal GVH disease which is radioresistant and can be adoptively transferred to syngeneic recipients.

Animals↗
PubMed2026

Integrated Cytokine and Immune Cell Profiling Reveals a Distinct Immune Signature Associated with High-Altitude Pulmonary Edema.

High-altitude pulmonary edema (HAPE) is a rapidly progressive, life-threatening disorder arising in otherwise healthy individuals upon ascent to high altitude, yet the mechanisms underlying maladaptive vascular leak remain poorly defined. Although elevated pulmonary arterial pressure and capillary stress failure are recognized as central hemodynamic drivers, accumulating evidence indicates that innate immune dysregulation is an equally critical, largely unexplored determinant of HAPE. To systematically delineate the immune and molecular programs that distinguish pathological responses to hypobaric hypoxia from acclimatization, peripheral blood along with clinical details was collected from low-altitude controls (LA-Cntrl, number of participants, (n = 19), healthy high-altitude sojourners (HA-Cntrl, n = 47), and HAPE patients (n = 90). Plasma proteomic markers were quantified using a targeted panel, while monocyte and dendritic cell subsets in peripheral blood mononuclear cells were immunophenotyped by multicolor flow cytometry. HA-Cntrl subjects displayed an anti-inflammatory profile, marked by the suppression of CXC chemokine receptor 3 axis chemokines. HAPE patients, in contrast, exhibited a pro-inflammatory, vascular injury signature, with elevated levels of inflammatory interleukins and myeloid and chemotactic factors. This inflammatory signature was accompanied by the expansion of classical monocytes, implicating a myeloid vascular program associated with HAPE.

Humans↗
PubMed2025

Immune Cell Type-Specific DNA Methylation Regions Associate With 24-Hour Blood Pressure Regulation in Black People.

BACKGROUND: DNA methylation and immune cells have been linked to blood pressure (BP) regulation and the development of hypertension. However, the immune cell profiles and the cell type-specific DNA methylation associated with BPs remain unclear. METHODS: This study evaluates the 19 cell type deconvolution algorithms using reduced representation bisulfite sequencing data, comparing them to in silico mixtures derived from whole-genome bisulfite sequencing. The top-performing algorithm, Epigenetic Dissection of Intra-Sample Heterogeneity (EpiDISH)-Robust Partial Correlations, was applied to 281 Black inpatients with 24-hour BP monitoring. The immune cell profiles and cell type-specific DNA methylation regions associated with these BP phenotypes were further investigated using regression analysis. RESULTS: In patients with hypertension, B-cell and CD4 effector memory T-cell abundances were significantly elevated. Monocyte and CD8 effector memory T-cell fractions positively correlated with nighttime BP, and CD3 T cells were inversely associated with office BP. These associations remained robust after covariate adjustments and were partially validated in the Medical Information Mart for Intensive Care-IV cohort. For the first time, we identified several cell type-specific DNA methylation regions as being associated with BP phenotypes and patterns across 13 immune cells, with approximately one third predominantly found in effector CD8 T cells. CONCLUSIONS: These findings provide novel insights into the epigenetically regulated immune mechanisms underlying BP regulation and identify potential targets for hypertension management.

Humans↗
PubMed2026

The Mediating Role of Immune Cells in the Genetically Predicted Relationship between Gut Microbiota and Puerperal Sepsis: A Mendelian Randomization Study.

INTRODUCTION: The causal relationship between gut microbiota and puerperal sepsis (PS) remains unclear, and there is a lack of in-depth research regarding the potential mediating role of immune cells in this context. OBJECTIVE: This study aims to investigate the causal relationship between gut microbiota and PS using Mendelian randomization (MR) analysis and to assess the mediating effects of immune cells on the risk of PS onset through mediation analysis. MATERIALS AND METHODS: We selected data from large-scale genome-wide association studies (GWAS) involving 473 gut microbiota species, 731 immune cell phenotypes, and PS datasets. Univariate MR (UVMR) analysis was employed to explore the causal relationship between gut microbiota and PS, with the primary statistical method being inverse variance weighting (IVW). Multiple statistical models were applied for sensitivity analysis to minimize the confounding effects of horizontal pleiotropy and heterogeneity. Subsequently, a two-step mediation MR analysis was conducted to evaluate whether immune cells mediate the relationship between gut microbiota and PS. RESULTS AND DISCUSSION: Analysis using various statistical models indicated that 11 gut microbiota species (e.g., Azorhizobium, Bacillus velezensis, CAG-245 sp000435175, Lentimicrobiaceae, and Providencia) exhibited a causal relationship with PS. Further reverse causal analysis between PS and gut microbiota ruled out the possibility of reverse causality. The two-step mediation MR analysis demonstrated that the percentage of IgD-CD27- B cells (10.26%) and CD62L- monocytes (17.29%) partially mediated the effect of CAG-245 sp000435175 on PS risk. CONCLUSION: This study provides evidence of a causal relationship between the abundance of certain gut microbiota species and PS, while also revealing a potential mediating role of immune cells. These findings offer valuable theoretical insights into personalized treatment strategies and the development of novel diagnostic biomarkers for PS.

Humans↗
PubMed2026

Spatial niche remodeling of senescent liver-resident immune cells and its role in chronic liver diseases.

The liver serves the triple functions of metabolism, detoxification, and immune surveillance. Its unique immune microenvironment is shaped by continuous exposure to gut-derived antigens, pathogen-associated molecular patterns (PAMPs), and metabolites arriving via the portal vein, necessitating a delicate equilibrium between immune tolerance and effector activation. This equilibrium relies on the coordinated activities of diverse liver-resident immune cell populations-including Kupffer cells (KCs), liver sinusoidal endothelial cells (LSECs), hepatic stellate cells (HSCs), dendritic cells (DCs), tissue-resident memory T cells (TRM), innate-like T cells, including mucosal-associated invariant T (MAIT) cells, natural killer T (NKT) cells, and γδ T cells, innate lymphoid cells (ILCs, encompassing conventional NK cells and helper ILC subsets), and neutrophils. With advancing age and chronic injury, these resident immune cell populations undergo profound senescence-associated phenotypic reprogramming that is spatially organized along the portal-to-central axis of the hepatic lobule. Key mechanisms include: telomere dysfunction and DNA damage accumulation driving persistent activation of p53/p21 and p16/Rb pathways; mitochondrial dysfunction with mitochondrial DNA (mtDNA) leakage fueling the senescence-associated secretory phenotype (SASP) via the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway; epigenetic age acceleration, including genome-wide H3K27me3 heterochromatinization; and metabolic reprogramming toward glycolysis and lipid accumulation. This review proposes a "spatial niche remodeling" framework to integrate these cell-intrinsic senescence programs with their lobular context, intercellular communication network rewiring, and pathogenic roles across the spectrum of chronic liver disease-from steatosis through steatohepatitis, fibrosis, cirrhosis, to hepatocellular carcinoma. We critically evaluate emerging senotherapeutic strategies targeting specific liver-resident immune cell subsets, discuss the barriers to clinical translation, and identify priority areas for future investigation, including the application of spatial multi-omics, humanized models, and epigenetic clock-guided clinical trials.

Kupffer cells↗
PubMed2026

A pancreatic cancer organoid-macrophage co-culture using starPEG-heparin hydrogel deciphers tumor-immune cell interactions.

Macrophages are among the most abundant immune cells in the pancreatic ductal adenocarcinoma (PDAC) tumor microenvironment (TME) and play a key role in regulating the immunosuppressive niche that facilitates tumor growth. Although recent three-dimensional (3D) culture systems using patient-derived materials have advanced our understanding of tumor biology, most models lack key cellular TME components and thus fail to capture tumor-immune cell interactions. To address this gap, we developed an in-vitro 3D co-culture model incorporating PDAC patient-derived organoids (PDOs) and macrophages within a synthetic hydrogel matrix. We optimized culture conditions by tuning medium and matrix conditions to support both cell lineages. Flow cytometry and transcriptomic analyses revealed that initially undifferentiated macrophages adopt an M2-like profile upon exposure to PDAC PDOs in starPEG-heparin hydrogels, mirroring the macrophage phenotypes observed by multiplex immunohistochemistry in the matched primary PDAC tissues. Cytokine secretome profiling revealed PDO-specific differences, indicating distinct underlying macrophage polarization subtypes. Collectively, our starPEG-heparin hydrogel-based 3D co-culture enables hypothesis-driven and physiologically relevant studies of tumor-macrophage interactions and may advance immune-modulatory treatment strategies in patients with PDAC.

Journal Article↗
PubMed2024

Inhibiting the expression of spindle appendix cooled coil protein 1 can suppress tumor cell growth and metastasis and is associated with cancer immune cells in esophageal squamous cell carcinoma.

Inhibiting the expression of spindle appendix cooled coil protein 1 (SPDL1) can slow down disease progression and is related to poor prognosis in patients with esophageal cancer. However, the specific roles and molecular mechanisms of SPDL1 in esophageal squamous cell carcinoma (ESCC) have not been explored yet. The current study aimed to investigate the expression levels of SPDL1 in ESCC via transcriptome analysis using data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus databases. Moreover, the biological roles, molecular mechanisms, and protein networks involved in SPDL1 were identified using machine learning and bioinformatics. The cell counting kit-8 assay, EdU staining, and transwell assay were used to investigate the effects of inhibiting SPDL1 expression on ESCC cell proliferation, migration, and invasion. Finally, the correlation between the SPDL1 expression and cancer immune infiltrating cells was evaluated by analyzing data from the TCGA database. Results showed that SPDL1 was overexpressed in the ESCC tissues. The SPDL1 expression was related to age in patients with ESCC. The SPDL1 co-expressed genes included those involved in cell division, cell cycle, DNA repair and replication, cell aging, and other processes. The high-risk scores of SPDL1-related long non-coding RNAs were significantly correlated with overall survival and cancer progression in patients with ESCC (P < 0.05). Inhibiting the SPDL1 expression was effective in suppressing the proliferation, migration, and invasion of ESCC TE-1 cells (P < 0.05). The overexpression of SPDL1 was positively correlated with the levels of Th2 and T-helper cells, and was negatively correlated with the levels of plasmacytoid dendritic cells and mast cells. In conclusion, SPDL1 was overexpressed in ESCC and was associated with immune cells. Further, inhibiting the SPDL1 expression could effectively slow down cancer cell growth and migration. SPDL1 is a promising biomarker for treating patients with ESCC.

Humans↗