Objective To explore the expression characteristics and clinical prognostic significance of tyrosine kinase binding protein（ TYROBP） gene in gliomas， providing a theoretical basis for developing targeted therapeutic strategics based on TYROBP. Methods This study conducted multidimensional analysis based on the Chinese Glioma Genome Atlas（ CGGA） and The Cancer Genome Atlas（ TCGA） databases. Firstly， a retrospective study was conducted on transcriptome sequencing data and corresponding clinical data from two independent cohorts in the CGGA database（ Dataset 1 containing 325 samples and Dataset 2 containing 693 samples） and one cohort in the TCGA database（ Dataset 3 containing 697 samples） to systematically investigate the relationship between TYROBP gene expression and patient clinical pathological characteristics. Concurrently， six surgical specimens of primary gliomas pathologically confirmed by the Department of Neurosurgery at Beijing Tiantan Hospital were collected between March and April 2025. Immunohistochemical techniques were employed to detect the expression distribution of the TYROBP in tumor tissues of different pathological types. Further research was conducted on the whole exome sequencing data of 286 glioma patients included in the CGGA database（ Dataset 4）. Based on the median TYROBP expression value（ M=148.56）， the cases were divided into TYROBP low expression group（ expression level ≤148.56， n=116） and TYROBP high expression group（ expression level＞148.56， n=115）， and the copy number variation characteristics and gene mutation spectrums were compared between the two groups. Survival analysis employed the Kaplan-Meier method to evaluate the association between TYROBP expression levels and patient overall survival， with its prognostic value validated through univariate and multivariate Cox proportional hazards models. In terms of mechanism exploration， functional enrichment analysis was performed on Dataset 1 to elucidate the biological processes involving genes co-expressed with TYROBP. The CIBERSORT algorithm was employed to quantitatively analyze the infiltration proportions of 22 immune cells within the tumor microenvironment， investigating the correlation patterns between various immune cell subpopulations and TYROBP expression. Results In Dataset 1， Dataset 2， and Dataset 3， the expression levels of the TYROBP gene increased with higher WHO grades （2-4）， with all differences being statistically significant（ F=38.379， 14.681， 76.724； all P＜0.01）. TYROBP expression levels were statistically higher in wild-type isocitrate dehydrogenase（ IDH） tumors compared to IDH-mutant tumors with 1p/19q deletion［ Dataset 1：（7.19±0.10） vs（. 5.55±0.11）（ F=54.120，P＜0.01）； Dataset 2： （7.54±0.11） vs.（ 6.54±0.10）（ F=25.151，P ＜ 0.01）， Dataset 3：（3.37±0.17） vs（ 3.07±0.17）（ F=171.19， P ＜ 0.01）］. Correlation analysis of clinical pathological characteristics revealed that TYROBP expression was statistically lower in primary tumors， low-grade tumors， and IDH-mutant cases with 1p/19q co-deletion compared to recurrent tumors， high-grade tumors， and non-IDH-mutant cases with 1p/19q co-deletion（ P ＜ 0.01）. The analysis of gene mutations and copy number changes in Dataset 1 showed that the mutation rates of E3 ubiquitin ligase 1 containing HECT and RLD domains（ HERC1）［ 4%（ 5/115）］ and thrombospondin type 1 domain containing protein 7B（ THSD7B）［ 4%（ 5/115）］ in the TYROBP high expression group were higher than those in the low expression group（ both 0%）， and the differences were statistically significant（ both χ2=4.117，both P＜0.05）. In Dataset 1， Dataset 2， and Dataset 3， the overall survival（ OS） of the TYROBP high expression group was shorter than that of the low expression group， with statistically significant differences （all P ＜ 0.05）. Multivariate Cox regression analysis showed that glioblastoma（ GBM）［ HR=2.218， 95%CI （1.438，3.422）， P＜0.001）， 1p/19q co-deletion［ HR=0.279， 95%CI（ 0.163，0.481），P＜0.01］， and TYROBP overexpression［ HR=1.582，95%CI（ 1.155， 2.168），P＜ 0.01］ were independent risk factors of the prognosis of glioma patients， and the differences were statistically significant. Functional enrichment analysis indicated that TYROBP participated in tumor microenvironment remodeling by regulating leukocyte-mediated immune responses and immunomodulatory processes. Correlation analysis revealed that this gene was positively correlated with the degree of M2 macrophage infiltration（ r=0.42， P＜0.001） and negatively correlated with the degree of initial CD4+ T cell infiltration（ r=-0.45，P ＜ 0.001）， with statistically significant differences. The expression of TYROBP was closely related to multiple key genes in leukocyte-mediated immunity. C1QA （r=0.924） and C1QC （r=0.904） were significantly positively correlated with TYROBP expression， and significantly negatively correlated with PIK3CB （r=-0.407） and PIK3R1 （r=-0.405）， with statistically significant differences（ all P ＜ 0.05）. Conclusions This study confirms that the expression pattern of TYROBP exhibits significant tumor type specificity. Its expression levels are not only closely associated with patient prognosis but also play a crucial role in regulating the tumor immune microenvironment. These findings provide a theoretical basis for developing targeted therapeutic strategies based on TYROBP.