Track and quantify key cytokines (e.g., IL-6, IFN-γ, GM-CSF) in real-time to evaluate CAR-T cell activation, toxicity potential, and immune modulation during preclinical or clinical studies.
Immune effector cell–associated neurotoxicity (ICANS) is a severe neurotoxic effect observed in patients receiving immune cell therapies such as CAR T-cell treatment. Understanding the complex neuroimmune interactions underlying ICANS remains a significant hurdle. Recent studies applying single-cell transcriptomics have highlighted the importance of dissecting neuroinflammatory cell populations at single-cell resolution to identify pathogenic subsets, transcriptional programs, and cytokine signaling patterns. These findings validate the power of Creative Biolabs' specialized sequencing service in driving targeted innovations in neuroimmune therapy development.
Are you currently facing the challenge of poorly understood mechanisms behind ICANS, inconsistent biomarkers, or ineffective therapeutic targets for neuroinflammation? Our single-cell RNA sequencing service of neuroinflammatory cell involved in ICANS helps you uncover actionable cellular signatures and regulatory pathways through high-resolution single-cell transcriptomics, enabling more precise intervention strategies in neuroimmune disorders.
Our service delivers real, actionable insights to accelerate your neuroinflammation research and immunotherapy development:
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Our approach prioritizes the identification of pathogenic immune subsets (e.g., myeloid cells, activated T cells) that contribute to ICANS. By focusing on transcriptional dynamics and cell-to-cell signaling within the CNS environment, we enable detailed stratification of inflammatory cell states.
Through gene expression profiling of cytokines, chemokines, and adhesion molecules at the single-cell level, we can map upregulated neuroinflammatory signaling pathways known to trigger vascular and neuronal damage during ICANS episodes.
Unbiased profiling facilitates identification of predictive biomarkers for ICANS risk, supporting patient stratification and therapeutic monitoring.
By contrasting transcriptional signatures between ICANS patients and controls, we can highlight regulatory nodes or immune checkpoints for intervention, aiding preclinical pipeline optimization.
Unlike general single-cell services, our solution is purpose-built for dissecting neuroinflammatory mechanisms specific to ICANS, integrating curated immune–neuro datasets and disease-relevant markers (e.g., IL-1β, GM-CSF, CCR2), providing high interpretability in translational neuroimmunology studies.
Our pipeline distinguishes fine-grained subsets such as activated microglia, perivascular macrophages, and infiltrating CCR5+ T cells, enabling insights into cellular crosstalk that contributes to blood-brain barrier (BBB) compromise and neuronal dysfunction.
We don't stop at cell clustering—our team delivers transcriptional network maps, pinpointing converging inflammatory pathways (e.g., TNF–NFκB, interferon-stimulated genes) that may serve as druggable targets or patient risk classifiers.
Our experienced immuno-neuro bioinformaticians provide 1:1 data review sessions, explain complex findings, and support integration into broader therapeutic or diagnostic programs.
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In patients experiencing ICANS following CAR T-cell therapy, differential gene expression analysis reveals distinct transcriptional alterations across six key immune cell types when compared to idiopathic intracranial hypertension (IIH). Multiple pro-inflammatory genes, including CXCL8, IL1B, and CCL3, are notably upregulated, particularly within monocytes and CD8+ T cells. Concurrent downregulation of regulatory or homeostatic genes is observed, suggesting a shift toward a heightened inflammatory state. These findings highlight cell type–specific immune activation patterns associated with ICANS onset and support the role of dysregulated cytokine signaling in its pathogenesis.
Fig.1 Differential expression reveals gene upregulation and downregulation across six cell types in ICANS onset versus IIH.1
What sample types are best suited for this service?
We accept CSF, PBMCs, and CNS tissue. CSF samples often yield the most disease-relevant immune subsets in ICANS studies.
Can I integrate this service with spatial or proteomic data?
Yes. We offer data compatibility with spatial transcriptomics and protein-level assays like CyTOF or ELISA.
What kind of report will I receive?
You'll receive a detailed analysis including cell type annotations, pathway insights, visual plots, and raw data files.
Is this service applicable beyond CAR T-induced ICANS?
Absolutely. This platform can support studies on multiple neuroinflammatory disorders (e.g., MS, paraneoplastic syndromes).
How does this compare to bulk RNA-seq of CSF or PBMCs?
Single-cell RNA-seq resolves individual cell behavior and minority cell subsets that bulk methods often miss, providing more actionable targets.
Track and quantify key cytokines (e.g., IL-6, IFN-γ, GM-CSF) in real-time to evaluate CAR-T cell activation, toxicity potential, and immune modulation during preclinical or clinical studies.
Accurately assess on-target/off-target binding across diverse tissues or cell types to ensure therapeutic antibody safety, efficacy, and translational relevance.
Creative Biolabs delivers precision solutions in neuroimmune research through high-resolution transcriptomics. Our single-cell RNA sequencing service of neuroinflammatory cell involved in ICANS is tailored to support your discovery, validation, and therapeutic development needs.
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Reference
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All products and services are For Research Use Only and CANNOT be used in the treatment or diagnosis of disease.
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