Search Results (1,659)

Background: Hashimoto’s thyroiditis (HT) is a common autoimmune disorder characterized by chronic inflammation and metabolic alterations. Mitochondria-derived peptides (MDPs), particularly mitochondrial open-reading frame of the 12S rRNA-c (MOTS-c), have emerged as key regulators of cellular metabolism, insulin sensitivity, oxidative stress, and inflammatory responses. This study aimed to investigate the association between circulating MOTS-c levels and HT and to explore its potential role in thyroid autoimmunity and metabolic regulation. Methods: In this cross-sectional study, patients diagnosed with HT (n: 90) were compared with age- and sex-matched healthy controls (n: 90). Results: A total of 180 participants were included, comprising 90 patients with HT and 90 age- and sex-matched healthy controls. Circulating MOTS-c levels were significantly lower in patients with HT compared to controls (p < 0.001). MOTS-c levels demonstrated significant inverse correlations with body mass index, fasting glucose, HbA1c, HOMA-IR, thyroid-stimulating hormone, C-reactive protein, and thyroid autoantibody levels (all p < 0.05). In subgroup analyses, these associations remained significant within the HT cohort, particularly for HOMA-IR and thyroid autoantibodies. Multivariable regression analysis identified HT (β = −30.04, p < 0.001) and HOMA-IR (β = −0.85, p < 0.001) as independent determinants of reduced circulating MOTS-c levels. Levothyroxine (LT4) use was not associated with significant differences in MOTS-c concentrations. Conclusions: Circulating MOTS-c levels are markedly reduced in patients with HT and are independently associated with insulin resistance and autoimmune burden. These findings suggest that impaired mitochondrial signaling may play a role in the pathophysiology of thyroid autoimmunity and highlight MOTS-c as a promising biomarker linking metabolic dysfunction and immune dysregulation. Full article

The hypothesis that Group A beta-haemolytic Streptococcus (GAS) triggers an autoimmune cascade targeting basal ganglia dopaminergic circuits—producing obsessive–compulsive disorder (OCD), tic disorders, or chorea depending on the receptor subtype involved—is biologically compelling and supported by emerging molecular evidence. Yet PANDAS has remained a diagnostic conundrum since its original description in 1998, with ongoing uncertainty surrounding diagnostic criteria, the interpretation of streptococcal serology, and the distinction from primary neurodevelopmental disorders. This study aimed to review the diagnostic challenges of PANDAS, with focus on streptococcal serology interpretation, advances in dopamine receptor autoantibody biology, the genetic epidemiology of primary tic disorders, and the differential diagnosis of acute neuropsychiatric presentations in children. A structured narrative review was conducted using PubMed, MEDLINE, EMBASE, and the Cochrane Library for publications from 1998 to early 2025 addressing PANDAS, PANS, streptococcal antibodies, childhood movement disorders, autoimmune encephalitis, and the genetics of tic disorders. No currently available biomarker—including ASO, anti-DNase B, anti-basal-ganglia antibodies, or the Cunningham Panel—has demonstrated adequate individual-level diagnostic accuracy for PANDAS. Emerging molecular evidence identifies anti-D1R autoantibodies, acting via G protein-and beta-arrestin-mediated signalling, as candidate biomarkers for PANDAS/PANS neuropsychiatric phenotypes, and anti-D2R autoantibodies for Sydenham chorea movement phenotypes; independent replication in unselected populations is required. Primary tic disorders carry heritability estimates of 50–80% and first-degree familial risk ratios of approximately 18-fold in large population-based cohorts. Prospective blinded studies have not demonstrated a consistent population-level association between GAS infections and tic or OCD exacerbations: PANDAS and PANS remain diagnoses of exclusion. The high background prevalence of both GAS exposure and primary neurodevelopmental disorders in overlapping paediatric age ranges creates conditions for incidental temporal co-occurrence. In the absence of validated molecular biomarkers, diagnostic imprecision carries direct clinical consequences: children may be exposed to treatments with significant risk profiles—including IVIG, plasma exchange, and prolonged antibiotic prophylaxis—while evidence-based therapies are delayed. A stepwise diagnostic approach incorporating the full differential diagnosis is both an epistemological and a patient safety imperative. Full article

Periodontitis (PD) and rheumatoid arthritis (RA) are chronic inflammatory disorders that impose substantial individual and societal burdens worldwide. PD is characterized by progressive destruction of the periodontal ligament and alveolar bone, leading to tooth loss, impaired oral function, and sustained systemic inflammatory burden. RA, affecting approximately 0.5–1% of the population, is a chronic autoimmune disease marked by persistent synovial inflammation, progressive joint destruction, disability, and reduced quality of life. Increasing evidence indicates that these conditions are biologically and clinically interconnected. Both diseases share key pathogenic pathways, including microbial dysbiosis, immune dysregulation, chronic inflammation, genetic susceptibility, and aberrant autoantibody responses. Particular attention has focused on keystone periodontal pathogens such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, which may promote protein citrullination and the formation of anti-citrullinated protein antibodies (ACPA), thereby providing a plausible mechanistic bridge between periodontal infection and systemic autoimmunity. Shared genetic risk factors, including HLA-DRB1 susceptibility alleles, further support a common host predisposition. Clinical, epidemiological, and translational studies increasingly support a bidirectional association. Individuals with PD appear to have a higher risk of RA development, whereas patients with RA demonstrate greater prevalence, severity, and progression of periodontal disease. Interventional studies suggest that nonsurgical periodontal therapy may reduce local periodontal inflammation, circulating inflammatory biomarkers, and RA disease activity indices, while effective pharmacological control of RA may also improve periodontal outcomes. This narrative review critically evaluates the PD–RA relationship across four interconnected domains: (i) epidemiological and clinical associations between PD and RA, (ii) key mechanisms underlying RA pathogenesis, (iii) shared biological pathways linking both diseases, and (iv) the extent to which treatment of one condition influences the other. Particular emphasis is placed on major sources of heterogeneity and confounding—including smoking, metabolic comorbidities, disease stage, therapeutic exposure, and variable diagnostic definitions—that may explain inconsistencies across the literature. By integrating current mechanistic and clinical evidence, this review provides a structured synthesis that extends beyond a descriptive overview of association studies. A clearer understanding of the periodontal–rheumatologic axis may facilitate risk stratification, identify novel therapeutic targets, and support integrated multidisciplinary care. Targeting both oral and systemic inflammation may improve outcomes in patients with coexisting PD and RA and may potentially reduce the risk or severity of one condition in individuals already affected by the other. Full article

Celiac disease (CD) is an autoimmune enteropathy of the small intestine affecting genetically susceptible individuals, characterized by an aberrant immune response to gliadin and sustained IgA-driven inflammation. IgA exists in two main subclasses, IgA1 and IgA2, which differ in distribution and function, but their profile in CD remains poorly characterized. Circulating free light chains (FLCs) are markers of B-cell activation and immune dysregulation, yet their role in CD has not been fully explored. The aim of this study was to characterize IgA subclasses and FLC profiles in newly diagnosed celiac patients. We analyzed sera from 108 CD patients and 29 healthy controls, assessing conventional serological markers (anti-tissue transglutaminase and anti-endomysial antibodies), together with total IgA, IgA1, IgA2, and FLC levels using a turbidimetric method. CD patients exhibited higher total IgA levels and an increased IgA1/IgA2 ratio, alongside a decreased k/λ ratio; these differences remained significant after adjustment for age and sex. When combined in a multivariable logistic model, these biomarkers yielded an AUC of 0.827, suggesting that the parameters identified in the univariate analyses provide complementary, non-redundant information that jointly highlights a reorganization of the humoral immune response. Due to the limited sample size, our results need confirmation in larger cohorts. However, our findings suggest a reorganization of the IgA compartment in CD, with selective expansion of IgA1 and preferential λ light chain usage, highlighting coordinated alterations in the humoral immune response. The integration of such markers, potentially in combination with -omics approaches, may contribute to a more refined and less invasive characterization of celiac disease. Full article

Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disorder arising from the convergence of genetic susceptibility, epigenetic remodeling, environmental exposures, and dysregulated immune networks. Although traditionally characterized by autoantibody production and immune complex mediated tissue injury, advances in genomics, systems immunology, and multi-omics profiling have revealed that lupus represents a multilayered failure of immune homeostasis driven by interconnected molecular circuits. Genetic variants enriched in regulatory immune enhancers establish a permissive transcriptional landscape that sensitizes innate nucleic acid sensing pathways and interferon signaling. Epigenetic remodeling further amplifies inflammatory transcriptional programs, while environmental triggers such as ultraviolet radiation and viral infection initiate bursts of nucleic acid release and immune activation. Defective apoptotic cell clearance, mediated in part by scavenger receptor dysfunction and complement abnormalities, increases the availability of immunogenic nucleic acids that engage pattern recognition receptors and drive chronic type I interferon production. This interferon-dominated environment rewires immune cell metabolism, alters differentiation trajectories of T and B lymphocytes, and sustains autoreactive immune circuits. Emerging multi-omics studies reveal distinct molecular endotypes defined by interferon signatures, metabolic states, and immune cell composition, highlighting the heterogeneity of disease mechanisms across patients. In this review, we integrate genetic, epigenetic, metabolic, and immunological insights to propose a systems-level model of lupus pathogenesis in which defective debris clearance, nucleic acid sensing, interferon amplification, and metabolic reprograming form a self-reinforcing pathogenic network. Understanding this integrated molecular architecture provides a foundation for biomarker-guided therapeutic strategies and precision medicine approaches aimed at disrupting the key nodes that sustain chronic autoimmunity in SLE. Full article

This study is a narrative review of natural killer (NK) cells in Behcet disease (BD). BD is an inflammatory disorder with manifestations in mucosal tissues. Unlike autoimmune diseases that generate autoantibodies, BD is believed to be an autoinflammatory disease triggered by innate immune cells rather than adaptive cells. Hyperactivation of neutrophils causes vasculitis and thrombosis, and they migrate into cutaneous and ocular lesions. Dominance of M1 macrophages promotes the differentiation of Th1 cells. Moreover, the cross-reaction of bacterial heat shock proteins induces production of cytokines such as IL-4 and IFN-γ in γδT cells, which alters the balance between Th1 and Th2 phenotypes. Nevertheless, NK cells play more critical roles in BD pathogenesis than other innate immune cells because not only is their activity precisely controlled by the interaction between ligands and receptors, but NK1 shift also elicits Th1 dominance. The genetic factors associated with BD are HLA-B51 and major histocompatibility complex class I-related chain A (MICA), which stimulate NK receptors as ligands. Improperly processed peptides dysregulate their interaction with NK receptors, triggering the inflammatory response. NK1 and NK2 subsets represent cytokine production in relapse and remission periods; however, the cytotoxicity of NK cells in relapse is lower than that in remission periods. It still remains unclear how NK cells are activated recurrently and expand cytokine production. This review highlights the regulation of gene expression encoding NK receptors, tissue-resident NK cells, and adaptive NK cells to discuss their potential for relapse. Splicing variants and readthrough genes encoding NK receptors easily alter cytokine production. Moreover, tissue-resident NK cells in mucosal tissues and adaptive NK cells that memorize the virus infection have the potential to trigger hyperactivation in relapse. Full article

This article discusses rheumatoid arthritis (RA) as a chronic, systemic autoimmune disease leading to progressive joint damage and multi-organ complications. The complex pathogenesis of the disease is presented, involving the interaction of environmental, genetic, and immunological factors, including the role of autoantibodies and proinflammatory cytokines. Particular attention is paid to leflunomide, a disease-modifying antirheumatic drug (DMARD), which primarily works by inhibiting the DHODH enzyme, leading to reduced T and B cell proliferation. The additional anti-inflammatory properties of the drug’s active metabolite, teriflunomide, and its impact on signaling pathways related to the immune response are also discussed. This article examines the variability in patient responses to leflunomide treatment in terms of both efficacy and toxicity, with particular emphasis on the potential role of pharmacogenetic factors. It was pointed out that polymorphisms in genes related to drug metabolism, transport, and mechanism of action may influence the pharmacokinetics and safety of the therapy. It was also emphasized that the available data are primarily derived from observational studies and small cohorts, and the results are often inconsistent. Although some genetic variants and plasma teriflunomide concentrations show potential as predictors of treatment response, the current level of evidence does not support the routine use of pharmacogenetic testing in clinical practice. The article emphasizes that the pharmacogenetics of leflunomide represents a promising, yet still exploratory, avenue of research in the context of personalized RA therapy. It emphasizes the need for larger, well-designed clinical trials and the development of standardized guidelines, which would be necessary before the potential implementation of such strategies in routine clinical practice. Full article

Background and Clinical Significance: NMDAR autoimmune encephalitis is a rare but potentially life-threatening autoimmune disorder that can be hard to recognize initially because it has nonspecific symptoms. In the early phase of the disease, clinical presentation is often dominated by psychiatric symptoms, which can be misleading. A diagnosis is established by demonstrating specific anti-NMDA receptor antibodies, with cerebrospinal fluid analysis considered the most reliable diagnostic method. Timely initiation of immunomodulatory therapy, including corticosteroids, intravenous immunoglobulins, and therapeutic plasmapheresis, significantly improves disease outcomes, while second-line therapies are used in refractory cases. Case Presentation: A 21-year-old female patient (M.B.) was admitted to the Psychiatry Clinic at the University Clinical Center of Vojvodina due to the sudden onset of behavioral changes, including social withdrawal, absence of verbal communication, and unusual orofacial grimacing. During hospitalization, the patient was intermittently in a state of severe psychomotor agitation and poorly communicative, with pronounced orofacial dyskinesias and involuntary tongue movements. Anti-NMDA receptor autoantibodies were detected in both serum and cerebrospinal fluid, and the patient was subsequently transferred to the Intensive Care Unit of the Neurology Clinic. Due to the lack of an adequate clinical response to pulse corticosteroid therapy, six cycles of therapeutic plasmapheresis were performed. Following this treatment, significant clinical improvement was observed. Conclusions: Timely recognition of this condition and a multidisciplinary approach allow for early initiation of immunomodulatory therapy and significantly improve treatment outcomes. Full article

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune dysregulation and multi-organ damage. Abnormal B cell activation and autoantibody production constitute the core pathological mechanism of SLE. However, the proportion, BCR pairing types, clonal evolution patterns, and transcriptomic features of dual BCR B cells in SLE remain incompletely elucidated. In this study, we employed single-cell RNA sequencing (scRNA-seq) combined with single-cell B cell receptor repertoire sequencing (scBCR-seq) to preliminarily analyze the proportion and characteristics of dual BCR B cells in SLE model mice (MRL/Lpr and SLE.Yaa) as well as in peripheral blood from SLE patients. The results showed: (1) Compared with control groups, the proportion of dual BCR B cells in SLE model mice and patients exhibited a decreasing trend, whereas the diversity of the CDR3 repertoire decreased and clonality increased. Increased clonal sharing was observed between single BCR B cells and dual BCR B cells. The main pairing types of dual BCR B cells were H + κ1 + κ2, H1 + H2 + κ, and H1 + H2 + κ + λ, with preferential utilization of autoimmunity-associated V gene families such as IGHV4-34, and high expression of IGHG subtypes. (2) Tracking analysis of B cell receptor clonality and effector molecule expression revealed that in SLE, dual BCR B cells tend to enrich in IFN-α/γ responses, TNF-NFκB inflammation, and complement pathways, and highly express interferon-related genes such as Ly6a, Isg15, MX1, and IFI6. (3) In both single BCR B and dual BCR B cells from SLE patients, the proportion of the naïve B cell subset decreased, whereas the proportions of plasma and Breg subsets increased and exhibited clonal expansion. SLE dual BCR Breg cells highly expressed IL10, HSPA1A, and others. This study is the first to reveal, at the high-throughput single-B-cell level, that the proportion, subset origin distribution, CDR3 repertoire composition, and effector molecule expression of dual BCR B cells display unique characteristics in SLE model mice and patients, providing baseline comparative data and novel research perspectives for further investigation into B cell effector functions and mechanisms in SLE patients. Full article

Background: Segmental arterial mediolysis (SAM) is a non-inflammatory vasculopathy that primarily affects the abdominal visceral arteries leading to hemorrhage, ischemia, or pseudoaneurysms. Its presentation can be mimicked by other vasculopathies including vasculitis involving the medium-sized blood vessels making it difficult to diagnose. Case Presentation: A 55-year-old woman presented with a two-hour history of sudden-onset, severe epigastric pain radiating to the chest. She was noted to be hypotensive with low hemoglobin 8.8 g/dL suspicious for a hemorrhagic cause. Her case was complicated by elevated international normalized ratio 3.7 in the setting of warfarin therapy for the mechanical mitral valve. The remainder of her complete blood count, complete metabolic panel, inflammatory markers, autoantibody serologies, and infectious testing were negative. Abdominal computed tomography angiogram revealed hemoperitoneum, bilateral renal infarctions, a large mesenteric hematoma, aneurysmal disease of the common hepatic and inferior mesenteric arteries, thrombosis and proximal dissection of the superior mesenteric artery, acute thrombosis of the left external iliac vein, and multiple sites of arterial extravasation from the pancreaticoduodenal artery and its branches. Mesenteric artery angiogram showed multivessel visceral artery aneurysms and stenoses characteristic of SAM for which she underwent transcatheter arterial embolization of the bleeding vascular bed. We provide a narrative literature review with a focus on common presentations and differentiating characteristics of vasculopathies that can involve medium-sized blood vessels. It is important to accurately diagnose SAM and its potential mimics as management strategies differ. Conclusions: SAM presents with medium vessel vasculopathy without vasculitis. Differentiation from mimics can be difficult but aided by familiarity of their characteristic findings and differentiating clinical characteristics. Full article

The autoantibody reactome refers to the multidimensional repertoire of antibody reactivities against self-antigens across the human proteome or selected antigenic compartments. This offers a scalable systemic layer for precision immunology across spontaneous autoimmunity and treatment-induced immune toxicity. Autoimmune diseases and immune-related adverse events (irAEs) share major features of dysregulated immunity, yet clinically useful tools for risk stratification, early detection, endotyping, and treatment guidance remain limited and slow. A central challenge is that tissue pathology is highly informative but not uniformly accessible across diseases and organ systems, whereas routine serology captures only a narrow fraction of immune heterogeneity. In this perspective, I argue that a global autoantibody reactome can serve as a central unifying framework linking systemic immune history, tissue pathology, and clinical trajectories across autoimmune disorders and irAEs. Rheumatoid arthritis (RA) provides a strong prototype because its serological diversity, major role of post-translationally modified autoantigens, and marked synovial heterogeneity allow reactome features to be interpreted against tissue biology. Immune checkpoint inhibitor-associated inflammatory arthritis serves as an illustrative rheumatic irAE and a model of treatment-induced immune dysregulation with clear opportunities for longitudinal blood-based profiling. Spatial transcriptomics and proteomics are therefore positioned not as stand-alone solutions, but as mechanistic tools that can decode reactome-defined immune states within tissue microenvironments where tissue is accessible. Clinical translation will require integration of autoantibody reactomes with tissue, circulating proteomic, imaging, genetic, and clinical data through transparent multimodal models, as well as a shift from exploratory resources such as AAgAtlas toward analytically validated and clinically interpretable biomarker panels for risk prediction, endotyping, monitoring, and biomarker-guided intervention. This perspective outlines technical and strategic steps toward clinically actionable decision support, including risk stratification before ICI initiation and treatment guidance for patients who develop ICI-induced inflammatory arthritis, through integration of autoantibody reactome profiling, spatial omics and transparent multimodal AI. Full article

Radon-222, a naturally occurring radioactive gas, is the second leading cause of lung cancer globally, after tobacco use. When inhaled, its decay products, especially polonium-218 and polonium-214, emit high-energy alpha particles that induce dense DNA damage in the bronchial epithelium. Because ambient radon measurements often vary significantly over time and across locations, they provide limited insight into individual exposure levels. This suggests the urgent need for biological markers that can accurately indicate internal dose and early signs of lung cancer development. This review offers an extensive overview of biomarkers associated with radon exposure, from internal dosimetry to early biological responses. It covers internal dose markers (e.g., radon progeny in air and ²¹⁰Po/²¹⁰Pb in bones and teeth), molecular and cytogenetic indicators of effective dose (such as chromosomal aberrations, γ-H2AX foci, and DNA adducts), and early effect markers (including somatic mutations, epigenetic changes, miRNA profiles, and autoantibody signatures). The review highlights translocations detected via FISH, discussing those that are stable over time versus those that are transient. It also evaluates the reliability and practicality of these biomarkers in occupational and residential settings, noting how smoking complicates causal inference due to overlapping mutation pathways. Finally, it suggests that integrating multi-omics technologies could improve the precision of biomarker panels. Full article

Background and Clinical Significance: Autosomal dominant tubulointerstitial kidney disease caused by a mutation in the uromodulin gene (ADTKD-UMOD) is a rare kidney disorder characterized by progressive tubulointerstitial damage and a slowly progressive loss of renal function. ADTKD is often under-recognized in the clinical setting. Diagnosis of ADTKD-UMOD can be challenging due to its nonspecific symptoms and is confirmed by genetic testing alone. Case presentation: We report the case of a 42-year-old male patient referred for evaluation of renal dysfunction, which was accidentally discovered during routine laboratory checks. He had no significant medical history and no known family history of kidney disease or gout. Physical examination was unremarkable. Renal dysfunction was confirmed, with serum creatinine at 1.44 mg/dL and eGFR at 59.5 mL/min/1.73 m². Urinalysis was within physiological limits, proteinuria being 75 mg/day. Uric acid was mildly elevated (7.5 mg/dL) without a history of gout. Other laboratory findings, including autoantibodies, were in the normal range. The patient underwent a kidney biopsy, though it was not diagnostic, showing mild focal tubular atrophy and interstitial fibrosis without glomerular involvement. Immunofluorescence staining was negative for complement and immunoglobulins. Given the above nonspecific findings, the patient was suspected of having possible ADTKD. Genetic investigation using a clinical exome next-generation sequencing approach identified a novel heterozygous missense variant in the UMOD gene (c.409T>C; p.Cysteine137Arginine (p.Cys137Arg)) that is likely pathogenic. The patient is under regular clinical-laboratory monitoring. After one year, his overall health is good, renal function is stable with no proteinuria, and uric acid is mildly increased without gout attacks. Conclusions: Increased clinical awareness is crucial for detecting ADTKD-UMOD. Genetic testing can help to resolve clinical diagnostic challenges in patients with unexplained decreased kidney function. Full article

Background/Objectives: Primary Sjögren’s disease is a systemic autoimmune disease characterized by chronic inflammation of exocrine glands and heterogeneous clinical manifestations. There remains a need for objective, non-invasive biomarkers that reflect local glandular involvement and disease-related immune activity. Methods: This observational cross-sectional case–control study included 34 patients fulfilling the 2016 ACR/EULAR classification criteria for primary Sjögren’s disease and 34 healthy controls between December 2024 and February 2025. Unstimulated whole-saliva samples were collected in the morning using the passive drool method, and salivary galectin-9 concentrations were measured via the enzyme-linked immunosorbent assay. Disease activity and symptom burden were assessed using validated indices, and receiver operating characteristic analysis was performed to evaluate discriminatory performance. Results: Salivary galectin-9 levels were significantly higher in patients with primary Sjögren’s disease compared with healthy controls. However, no significant associations were observed between salivary galectin-9 levels and disease activity scores after correction for multiple comparisons, nor with patient-reported symptoms, autoantibody profiles, Schirmer test results, or minor salivary gland biopsy findings. Salivary galectin-9 demonstrated limited discriminative ability between patients and controls. Conclusions: Salivary galectin-9 levels were elevated in primary Sjögren’s disease and may be associated with local glandular immune processes. Further prospective studies are needed to determine their clinical relevance. Full article

Avian ganglioneuritis is one of the most widespread diseases of psittacines and is caused by parrot bornavirus (PaBV). It has been suggested that PaBV causes a T-cell-mediated immunopathology comparable to Borna disease virus 1 (BoDV-1). However, the factors involved in progression from infection to clinical disease in psittacines remain poorly understood. It has been proposed that autoantibodies directed against endogenous gangliosides of the central and peripheral nervous systems contribute to disease development. These anti-ganglioside antibodies have been suggested as potential diagnostic markers for birds developing clinical avian ganglioneuritis independent from the causing infectious agent. In this study, 257 plasma samples from cockatiels (Nymphicus hollandicus) experimentally infected with PaBV, with known infection status as well as defined clinical and postmortem outcomes, were submitted in a blinded manner to a commercial laboratory for anti-ganglioside antibody testing. The results were compared with the presence of anti-PaBV antibodies, clinical signs, gross pathological findings, and histopathological results. Among 25 birds with dilated proventriculi at the time of necropsy, 9 (36%) tested positive for anti-ganglioside antibodies, whereas 16 (64%) tested negative. Of 56 birds with histopathological avian ganglioneuritis, 26 (46.43%) tested positive and 30 (53.57%) tested negative. Among 33 birds without histopathological inflammatory lesions, 19 (57.58%) tested negative and 14 (42.42%) tested positive. These results indicate that no association between the occurrence of avian ganglioneuritis and the detection of anti-ganglioside antibodies was seen. Full article