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Background Pediatric brain tumors are the leading cause of cancer-related mortality in children and comprise a heterogeneous group of malignancies. Among these, pediatric high-grade gliomas (pHGG) remain some of the most aggressive and treatment-resistant tumors with poor long-term outcomes. While immunotherapeutic efforts have largely focused on T cells, the diverse roles of B cells in the tumor microenvironment (TME), specifically within the central nervous system, remain poorly understood.Methods Our lab developed a method for reconstructing B cell receptor (BCR) repertoires from non-targeted bulk RNA sequencing data using bcRflow, a Nextflow pipeline. We applied this approach to transcriptomic data from over 2,000 pediatric brain tumor samples, including more than 250 pHGG samples stratified by key genetic subtypes. We assessed class switch recombination (CSR) and somatic hypermutation (SHM) rates, isotype distribution, clonal expansion, and repertoire diversity. Clones were then stratified into small, medium, large, and hyperexpanded categories based on relative abundance.Results Our analysis of BCR repertoires in pHGG samples revealed moderate to low diversity compared to other pediatric brain tumor types. This suggests a restricted B cell response within the pHGG microenvironment, potentially reflecting chronic antigen exposure or immune exhaustion. These samples demonstrated dominance of hyperexpanded, clonally restricted B cell populations, indicating that while certain clones are proliferating, they may be functionally impaired in the context of tumor clearance. CSR was limited, and SHM rates were low across isotypes relative to other tumor types, suggesting incomplete B cell maturation and a dysregulated activation state. Analysis of the occupied repertoire space revealed that the B cell compartment is dominated by moderately abundant clones, primarily within the [1–10] and [11–100] frequency bins, rather than a diverse spread. Additionally, CDR3 homology analysis uncovered discrete clusters of sequence similarity, suggesting that B cell responses may be converging on shared antigenic epitopes present across multiple pediatric brain tumor types.Conclusions These findings depict a constrained and potentially dysfunctional B cell landscape in pHGG, raising questions about whether these cells contribute to anti-tumor immunity, immune evasion, or represent a non-productive adaptive response. Within the immunosuppressive TME, the observed clonal restriction and low diversity suggest B cells may be responding to chronic antigen exposure without effective clearance. These insights underscore the need for more comprehensive multi-omics approaches to define B cell phenotypes and therapeutic relevance. Understanding how B cells interact with the broader immune landscape in pHGG could ultimately support the development of B cell-leveraging immunotherapies to combat these devastating cancers.