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At least 19 recordsLinked to original sources
PubMedDate not supplied

Joseph E. Smadel Memorial Lecture: neuroimmunologic diseases of animals and humans.

New precepts gained from the crescendo of neuroimmunobiologic research of recent decades have increased our understanding of experimental allergic encephalomyelitis (EAE), virus-associated acute disseminated encephalomyelitis (ADE), and multiple sclerosis (MS). EAE of animals and humans provides evidence of the existence in mammalian lymphoid tissues of potential clones of cells with autoreactivity for myelin basic protein (MBP) and other antigenic constituents of the central nervous system (CNS). In a new hamster model, EAE has been strikingly potentiated by persistent infection of the CNS with defective measles virus, a finding that also has implications for virus-associated ADE. Endogenous MBP or MBP degradation fragments, reactive with MBP antibodies of various affinities, have been detected by a recently devised radioimmunoassay in serum, plasma, and other body fluids of normal rats, rats with EAE, and patients with virus-associated ADE or MS. Circulating MBP or MBP fragments may be of great importance in inhibiting neuroautoimmune reactivity and play a role in repair of immunologic CNS injury should it inadvertently occur. Finally, the impressive degree of concordance of immunologic events in EAE, virus-associated ADE, and MS provides additional support for the central importance of host neuroimmunologic responses in the pathogenesis of these neutologic diseases.

Animals↗
PubMedDate not supplied

Neuroimmunology of Alzheimer's disease: a conference report.

A multidisciplinary group met under the auspices of the National Institute on Aging and the Dell Foundation at the Princess Resort in San Diego, CA on April 5-6, 1991. The meeting was organized by Dr. Caleb E. Finch, University of Southern California, Dr. Zaven Khachaturian, National Institute on Aging, Dr. William Markesbery, University of Kentucky, Dr. Patrick McGeer, University of British Columbia, and Dr. Joseph Rogers, Institute for Biogerontology Research, and covered recent data suggesting neuroimmune correlates of Alzheimer's disease (AD). These findings span many of the major immune system phenomena, from major histocompatibility complex (MHC) antigens through cytokines and the complement cascade and suggest that some facets of AD pathogenesis may be immune related.

Alzheimer Disease↗
PubMed1992

The neurobiology of tumours and head injury, and the neuroimmunology of central nervous system malignancy.

The application of modern investigative techniques in molecular biology, cytogenetics and immunocytochemistry has yielded much new information on central nervous system tumours both in vitro and in vivo. Although the clinical potential of these findings is yet to be fully realized, preliminary clinical studies based on this new information are now in progress. The mechanisms and consequences of brain damage in head injury have been studied both clinically and experimentally for many years; new investigative techniques focusing on the cellular and subcellular basis of brain damage have provided information which is interesting not only in terms of basic neurobiology but also in the identification of new areas for possible therapeutic intervention.

Brain Damage, Chronic↗
PubMed1976

[Basic principles and application of cerebrospinal fluid immunoelectrophoresis].

The basic principles, prerequisites, and limitations of the immunoelectrophoresis of the cerebrospinal fluid are discussed. Major emphasis has been placed on the characteristics of normal and pathological immunoelectropherograms of the liquor cerebrospinalis as well as on the results of studies of inflammatory and neuroimmunological diseases. The detection of a barrier profile, the method of determining special qualitative alterations of immunoglobulins of the liquor cerebrospinalis due to neuroimmunological diseases, and additional applications are discussed in detail. The procedure has been critically reviewed because the results obtained are, for the most part, of a general and nonspecific character and the method cannot be standardized adequately and also does not yield sufficient quantitative data. The advantages (differentiated qualitative changes) and disadvantages (technique troubles) are pointed out.

Blood-Brain Barrier↗
PubMed1976

[Demonstration of a factor in cerebrospinal fluid with inhibitory activity for electrophoretic cell mobility in multiple sclerosis (author's transl)].

Inhibition of electrophoretic cell migration using cerebrospinal fluid (CSF) directly was investigated by the modified MEM (macrophage electrophoretic mobility) and TEEM (tanned sheep erythrocyte electrophoretic mobility) tests, respectively. An inhibitory activity of macrophage slowing factor (MSF)--one of in vivo lymphokines--in CSF was established in cases of multiple sclerosis (17.5 +/- 3.8%), and neurolues. The value of this MSF assay turned out to be significantly different from the remaining inflammatory ailments of the nervous system (10.1 +/- 6.8%). Results of other neurological diseases were found to be very much lower (5.1 +/- 4.2%). It seems important, for immunopathogenesis and the diagnosis of neuroimmunological diseases with enhanced cellular immunoreaction, to evaluate MSF activity in CSF. To characterize the active factor in CSF (and serum) these fluids were fractionated by gel filtration chromatography as well as supernatants from lymphocyte-antigen incubation in MS patients. The main activity for inhibition of electrophoretic cell mobility was eluated in the same fraction in these fluids. It could be shown that units have a molecular weight of about 15000 Daltons; this value for MSF lies below those for other inhibitory lymphokines.

Erythrocytes↗
PubMed1992

Human astroglial but not microglial cells synthesize alpha 2-macroglobulin in vitro.

Alpha 2-macroglobulin (alpha 2M) is a serum proteinase inhibitor with a broad specificity. At present its role in human brain is unknown, but recent data report its presence in the CNS, particularly at glial level. Previous studies from our group demonstrated the synthesis and secretion of alpha 2M in different glial cultures derived from an astrocytoma and a glioblastoma. In the present study a human fetal astroglial cell line and two microglial established cell lines are examined for the presence of alpha 2M by using polyclonal antibodies in ELISA and immunofluorescence assays. While we observed a strong specific positivity in the cytoplasm and in the culture medium of the GFAP, vimentine positive cells, no positivity was detected in FcR, lysozyme positive microglial cells. Since interaction of proteinases and proteinase inhibitors appear to play a crucial role in the development of neuroimmunological competence, these data suggest a dissociation of macro and micro-glia immune functions.

Astrocytes↗
PubMed1992

The association of cervical spondylosis and multiple sclerosis.

The diagnostic and therapeutic considerations produced by the coexistence of cervical spondylosis and multiple sclerosis are complex. We have encountered six patients, affected by both multiple sclerosis and cervical spondylosis, in whom neurosurgical procedures were performed. The diagnosis of multiple sclerosis was confirmed by a combination of clinical, neuroimmunologic, electrophysiologic, and neuroradiologic findings. The diagnosis of spondylosis with spinal cord compromise was confirmed by myelography and computed tomographic scan in all cases, and by magnetic resonance imaging in four. Surgery was followed by lasting clinical improvement in two patients, transient improvement in one, and no change in the other three. Our experience confirms that multiple sclerosis and cervical spondylosis can coexist and suggests that this coexistence may result in an interaction that compounds the deleterious effect on the nervous system. Diagnostic evaluations of patients, particularly young patients, with symptoms of cervical spondylosis should include consideration of the possible coexistence of multiple sclerosis. The evaluation of a patient with known multiple sclerosis who develops new signs of cervical spinal cord dysfunction should always include spinal neuroimaging studies. When progression of symptoms coincides with documented progression of anatomic compression, surgical intervention can yield good results.

Adult↗
PubMed1992

Neurological consequences of immune dysfunction: lessons from HIV infection and multiple sclerosis.

In a recent workshop held on Sanibel Island, Florida (18-21 January 1992), the two most common neuroimmunologic diseases of young adults, multiple sclerosis (MS) and HIV encephalopathy, were jointly discussed. The logic of assembling investigators from these two fields was based not on an assumed etiologic connection between MS and retroviral infection of the central nervous system (CNS), but rather in the hope of uncovering potential common pathogenic mechanisms, particularly as might relate to trafficking of mononuclear cells into the central nervous system, the distribution and function of macrophages and microglia, the structure and function of the blood-brain barrier, and the role of cytokines released by activated cells. Multiple sclerosis is a disease without a known etiologic agent or pathogenesis. While the causative agent for HIV leukoencephalopathy is known, the pathogenesis of the disease remains entirely enigmatic (a topic covered by R. Johnson). This meeting brought together two different groups of investigators to compare and contrast the diseases and to share perspectives, paradigms, and data with the aim of cross-fertilizing the disciplines and generating healthy hybrids.

Acquired Immunodeficiency Syndrome↗
PubMed2025

Genetic Landscape of Opsoclonus-Myoclonus-Ataxia Syndrome in Children.

BACKGROUND: Opsoclonus-myoclonus-ataxia syndrome (OMAS) is a rare neurological disorder, with involuntary rapid saccadic conjugate eye movements as one of characteristics, primarily affecting the cerebellum. While the exact pathogenesis remains unclear, genetic and autoimmune factors have been suggested to contribute to its development. METHODS: We enrolled patients diagnosed with OMAS before the age of 18 years at a pediatric neuroimmunology clinic in Boston, United States, using the 2004 Genoa Criteria. Whole genome sequencing was conducted for the patients and their biological parents in all cases, with one case including an unaffected twin sibling. RESULTS: De novo germline variants (DNVs) in probands were identified and validated and analyses of structural variants, recessive variants in neuroimmune-associated genes, and high-resolution human leukocyte antigen (HLA) typing were performed. Our study included 42 patients, 23 of whom had neuroblastoma. We found 12 confirmed DNVs in protein-coding regions in nine patients (29.0% of 31 from 30 trios and 1 quartet). Ten patients (23.8% of 42) had rare homozygous or compound heterozygous variants known to alter protein function, affecting 11 genes. Notably, the major histocompatibility complex, class II, DR beta 1 (HLA-DRB1) &#x2217;01 allele was observed in 27 out of 84 (32.1%) alleles in the patients, significantly higher than that in the general population (chi-square test, P < 0.0001). In one case, a potential genetic modifier of OMAS with severe cerebellar atrophy was identified, associated with a protein-truncating DNV in the CACNA2D2 gene. CONCLUSIONS: This first genome sequencing study reveals potential genetic contributors to OMAS, implicating polygenic predisposition-with HLA-DRB1&#x2217;01 as a possible factor-combined with nongenetic risk factors like neuroblastoma.

Humans↗
PubMed2025

Immune dysfunction in Alzheimer disease.

Emerging evidence highlights the crucial role of peripheral immune cells in maintaining brain homeostasis and their influence on the pathology of Alzheimer disease (AD). Genome-wide association studies have identified numerous AD risk variants in genes expressed by immune cells, implicating innate and adaptive immune pathways in disease progression. Advances in neuroimmunology have revealed that immune cell crosstalk involving T cells, B cells, monocytes&#xa0;and/or&#xa0;macrophages and neutrophils can modulate the hallmark features of AD, including amyloid plaque accumulation, tau pathology and chronic neuroinflammation. Mechanistic insights suggest that chronic peripheral inflammation, immune exhaustion, metabolic dysfunction and epigenetic reprogramming exacerbate neurodegeneration in AD by promoting toxic inflammation and impairing protein clearance in the brain. These findings may catalyse the development of novel immunomodulatory strategies, such as immune checkpoint inhibition and cytokine targeting, among others, for AD. This Review examines peripheral immune alterations in AD, evaluates related therapeutic opportunities and highlights key knowledge gaps, particularly the need for human-derived data to advance translational progress. Future research should prioritize personalized approaches that integrate genetic risk, immune profiling and ageing to inform next-generation therapies for AD.

Humans↗