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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE189743 | GEO | 2023/08/01

REPOSITORIES: GEO

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Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma.

Project description:Neuroblastoma is a lethal childhood solid tumor of developing peripheral nerves. Two percent of children with neuroblastoma develop opsoclonus myoclonus ataxia syndrome (OMAS), a paraneoplastic disease characterized by cerebellar and brainstem-directed autoimmunity but typically with outstanding cancer-related outcomes. We compared tumor transcriptomes and tumor-infiltrating T and B cell repertoires from 38 OMAS subjects with neuroblastoma to 26 non-OMAS-associated neuroblastomas. We found greater B and T cell infiltration in OMAS-associated tumors compared to controls and showed that both were polyclonal expansions. Tertiary lymphoid structures (TLSs) were enriched in OMAS-associated tumors. We identified significant enrichment of the major histocompatibility complex (MHC) class II allele HLA-DOB∗01:01 in OMAS patients. OMAS severity scores were associated with the expression of several candidate autoimmune genes. We propose a model in which polyclonal auto-reactive B lymphocytes act as antigen-presenting cells and drive TLS formation, thereby supporting both sustained polyclonal T cell-mediated anti-tumor immunity and paraneoplastic OMAS neuropathology.

| S-EPMC10551040 | biostudies-literature

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [TCR-Seq]

Project description:Two percent of children with Neuroblastoma, a pediatric solid tumor of the peripheral nerve ganglia, develop Opsoclonus Myoclonus Ataxia Syndrome (OMAS), a paraneoplastic disease characterized by devastating cerebellar and brainstem-directed autoimmunity, but typically with outstanding cancer-related outcomes. Here, we compared tumor transcriptomes and tumor infiltrating T- and B-cell repertoires from a cohort of OMAS subjects with neuroblastoma to a set of controls from 13 low- and 13 high-risk non-OMAS associated neuroblastoma tumors.

2023-08-01 | GSE189742 | GEO

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [BCR-Seq]

2023-08-01 | GSE189741 | GEO

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [RNA-Seq]

2023-08-01 | GSE189367 | GEO

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma

Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma

| PRJNA784301 | ENA

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [RNA-Seq]

Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [RNA-Seq]

| PRJNA782665 | ENA

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [BCR-Seq]

Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [BCR-Seq]

| PRJNA784304 | ENA

Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [TCR-Seq]

Project description:Polyclonal lymphoid expansion drives paraneoplastic autoimmunity in neuroblastoma [TCR-Seq]

| PRJNA784303 | ENA

Paraneoplastic neuronal intermediate filament autoimmunity.

Project description:ObjectiveTo describe paraneoplastic neuronal intermediate filament (NIF) autoimmunity.MethodsArchived patient and control serum and CSF specimens were evaluated by tissue-based indirect immunofluorescence assay (IFA). Autoantigens were identified by Western blot and mass spectrometry. NIF specificity was confirmed by dual tissue section staining and 5 recombinant NIF-specific HEK293 cell-based assays (CBAs, for α-internexin, neurofilament light [NfL], neurofilament medium, or neurofilament heavy chain, and peripherin). NIF-immunoglobulin Gs (IgGs) were correlated with neurologic syndromes and cancers.ResultsAmong 65 patients, NIF-IgG-positive by IFA and CBAs, 33 were female (51%). Median symptom onset age was 62 years (range 18-88). Patients fell into 2 groups, defined by the presence of NfL-IgG (21 patients, who mostly had ≥4 NIF-IgGs detected) or its absence (44 patients, who mostly had ≤2 NIF-IgGs detected). Among NfL-IgG-positive patients, 19/21 had ≥1 subacute onset CNS disorders: cerebellar ataxia (11), encephalopathy (11), or myelopathy (2). Cancers were detected in 16 of 21 patients (77%): carcinomas of neuroendocrine lineage (10) being most common (small cell [5], Merkel cell [3], other neuroendocrine [2]). Two of 257 controls (0.8%, both with small cell carcinoma) were positive by both IFA and CBA. Five of 7 patients with immunotherapy data improved. By comparison, the 44 NfL-IgG-negative patients had findings of unclear significance: diverse nervous system disorders (p = 0.006), as well as limited (p = 0.003) and more diverse (p < 0.0001) cancer accompaniments.ConclusionsNIF-IgG detection by IFA, with confirmatory CBA testing that yields a profile including NfL-IgG, defines a paraneoplastic CNS disorder (usually ataxia or encephalopathy) accompanying neuroendocrine lineage neoplasia.

| S-EPMC6207411 | biostudies-literature

Fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-09-16 | E-GEOD-71084 | biostudies-arrayexpress