PubMed Health⌕ Search

Biomedical subjects

B Giometto

Publications and source records attributed to B Giometto.

51 records · Page 3Linked to original sources
PubMed1995

The costimulatory molecule B7 is expressed on human microglia in culture and in multiple sclerosis acute lesions.

B7 is a costimulatory molecule which is expressed on antigen-presenting cells and which plays a pivotal role in T cell activation and proliferation. To elucidate mechanisms regulating intracerebral immune responses, expression of B7 was examined in cultured microglial cells and in brain tissue from control and multiple sclerosis patients. Using immunocytochemical and polymerase chain reaction techniques, we show that B7 was expressed in cultured microglial cells from the human embryonic brain. Microglia also bound the soluble form of the B7 receptor CTLA-4 (CTLA-4-Ig). B7 gene expression and binding of anti-B7 antibodies and CTLA-4-Ig increased after treatment with interferon-gamma. B7 was not inducible in human astrocytes. Human microglia expressed other costimulatory molecules, such as intercellular adhesion molecule-1, LFA-1 and LFA-3. In sections of multiple sclerosis brains, B7 immunoreactivity was detected on activated microglia and infiltrating macrophages within active lesions. In chronic lesions, only perivascular cells were stained. B7 immunoreactivity was undetectable in sections from Alzheimer's disease or normal brain tissue. These data suggest that B7 may be involved in T cell activation and lesion development in multiple sclerosis and that the regulated expression of B7 on microglia may contribute to the local stimulation of T cell proliferation and effector functions.

Acute Disease↗
PubMed1994

Circulating autoantibodies against central nervous system (CNS) antigens in neurological diseases.

A number of investigators have reported the detection of circulating autoantibodies directed against serum and cerebrospinal fluid (CSF) neuronal antigens in certain neurological clinical conditions. Using an immunohistochemical technique, we examined the sera and (when available) the CSF from 120 patients with several neurological disorders and 40 controls in order to analyze the incidence and specificity of the detection of these autoantibodies. Circulating autoantibodies were found in 3 patients with cerebellar degeneration and in 3 patients with stiff-man syndrome, and different staining patterns were revealed in the same disease. Our findings confirm the reported disease-specificity of the detection of these autoantibodies in biological fluids, suggesting that a standardized immunohistochemical technique could constitute an easy and reproducible diagnostic tool in selected neurological conditions. These procedures enable the identification of an immunological pathogenesis of the disease and, in some case, early cancer detection. When atypical staining patterns of staining are found at immunohistochemistry, Western blot characterization of the recognized neuronal antigens is recommended.

Aged↗
PubMed1994

Cerebrovascular and neurological disorders associated with antiphospholipid antibodies in CSF and serum.

Paired serum and cerebrospinal fluid (CSF) samples from 70 patients with inflammatory and non-inflammatory neurological diseases, as well as 10 sera from patients with primary antiphospholipid syndrome (PAS), six of which presented with cerebrovascular ischemic syndromes, were studied for the presence of anticardiolipin antibodies (ACA) of the G and M classes. PAS sera and some selected paired CSF and serum specimens, were also analyzed for the presence of anti-phosphatidylserine (PS) and anti-phosphatidylethanolamine (PE) antibodies. High levels of IgG and IgM ACA were synthesized intrathecally only in patients with neurosyphilis. Patients with other infectious or inflammatory neurological diseases very rarely showed detectable levels of ACA in serum and/or CSF. ACA were found not only in patients with untreated PAS but also in the serum of 3/7 patients with migraine, thus confirming a relationship between ACA and vascular disorders. The search for PS and PE antibodies disclosed that in PAS patients the serum titers of these antibodies mirrored ACA IgG and IgM titers, while they were never found in the CSF.

Adolescent↗
PubMed1992

Growth factor (M-CSF) and antigenic properties of macrophages in meningioma.

In meningiomas, transformed meningeal cells can share morphological aspects (in hemangiopericytic meningioma) and antigenic properties (i.e.: HLA-DR antigens expression) with elements of the monocyte/macrophage lineage. In this report, we describe a case of a highly vascular meningioma where numerous tumor cells, studied with immunohistochemical methods, present phenotypic properties of macrophages. Moreover, the cerebrospinal fluid (CF) analysis disclosed, using a biological assay, a high level of a growth factor for monocytic elements, the Macrophages Colony Stimulating Factor (M-CSF). Our findings may confirm that transitional aspects between different mesenchymal cells could be present in meningiomas.

Antigens, CD↗
PubMed1992

On the role of interleukin-2 (IL-2) in multiple sclerosis (MS). IL-2-mediated endothelial cell activation.

Increased serum levels of IL-2 and sIL-2R can be demonstrated in patients with active MS, a finding that strongly supports the hypothesis of a systemic T cell activation in such patients. However, IL-2 may play a crucial role in MS immunopathology by activating endothelial cells, as suggested by the vascular leak syndrome complicating hrIL-2 therapy. Early BBB impairment and focal perivascular edema that characterize MS lesions may be the effect of an IL-2-induced cytokine cascade.

Blood-Brain Barrier↗
PubMed1991

Macrophages in human sensory ganglia: an immunohistochemical and ultrastructural study.

The paper describes the immunohistochemical and ultrastructural features of normal posterior root ganglia in a group of humans aged 1 day to 80 years and compares the findings with those seen in the ganglia of normal rats of various ages, some of which underwent permanent traumatic lesions of the sciatic nerve. In humans, cells with the immunohistochemical reactions of macrophages are present in small number at birth, most of them having an endoneurial position. Subsequently, their number increases and more of them are seen around neurons, where their processes intermingle with those of satellite cells. Ultrastructural studies confirm that, in addition to interstitial cells, a small number of cells in satellite position have features of mesenchymal cells. In this respect, human sensory ganglia differ from those of rodents and this difference may explain why no nodules of Nageotte can be found either in ageing animals or after a permanent damage to the nerve has produced considerable cell loss. Other features observed in human ganglia, but absent in rats, are multiple layers of satellite cells surrounding each neuron and desmosome-like structures between satellite cell processes. Previous studies describing maturation of the satellite-nerve cell complex in animals are confirmed. In addition, the present investigation shows that, in human ganglia, satellite cells acquire a more elaborate structure than in rodents. It is also suggested that mesenchymal cells may play a role in the trophism of nerve cells and their removal after irreversible damage.

Adolescent↗
PubMed1990

Transferrin receptors in rat central nervous system. An immunocytochemical study.

Using an immunocytochemical method we demonstrated the presence of TfR on adult rat neurons, particularly in the cerebral cortex and brain stem. The monoclonal antibody (mab) against rat TfR (clone OX 26) stained neurons of all cortical layers and in the brain stem where the reaction was most evident. Purkinje cells in the cerebellum and scattered neurons in the gray matter of the cervical spinal cord were weakly stained. Choroid plexus cells also reacted with the mab against TfR whereas oligodendrocytes in the cerebral white matter were faintly outlined by the mab. The presence of TfR on endothelial cells of brain capillaries was here confirmed.

Animals↗
PubMed1989

Immune activation in multiple sclerosis: study of IL-2, sIL-2R, and gamma-IFN levels in serum and cerebrospinal fluid.

Serum and cerebrospinal fluid (CSF) levels of interleukin-2 (IL-2), soluble IL-2 receptor (sIL-2R), and gamma-interferon (gamma-IFN) were measured in multiple sclerosis (MS) patients, human immunodeficiency virus type 1 (HIV-1)-infected patients and normal controls (NC). Increased levels of both IL-2 and sIL-2R were found in MS serum. Moreover, 11 of 50 MS patients showed detectable levels of IL-2 in the CSF. HIV-1-infected patients had increased levels of sIL-2R in serum and, less frequently, in the CSF. gamma-IFN was never detected in serum and CSF of all the patients studied. These findings confirm preliminary reports, further stress a systemic T-cell activation in MS, and support the hypothesis that an immunologic disorder exists in such patients.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Acute-phase proteins in Alzheimer's disease.

The main 'acute-phase proteins' were determined in serum of 20 patients with presenile Alzheimer's disease (AD) and compared with values in 18 age-matched healthy control subjects. Following parameters were evaluated: alpha 1-antitrypsin (alpha AT), haptoglobin (HPT), transferrin (TRF), acidic alpha 1-glycoprotein (A alpha G), ceruloplasmin (CER), alpha 2-macroglobulin (alpha MG), C-reactive protein (CRP), albumin (ALB), together with the immunoglobulins IgG, IgM and IgA, and some of the most significant factors of the classic (C3, C4) and alternative (properdin factor B) pathways of complement activation. The results showed a statistically significant increase in the levels of alpha AT (p less than 0.001), CER (p less than 0.001) and of all the complement factors studied (p less than 0.005). The levels of other acute-phase protein (HPT, TRF, A alpha G, alpha MG, CRP, ALB) and immunoglobulins (IgG, IgM, IgA) were similar in AD patients and normal controls. These results give rise the possibility that these elements indicate an altered immunoregulation compatible with chronic cell damage and/or chronic inflammation conditions. Moreover, the increased level of alpha AT can be related to the low production of interleukin-1 (IL-1) reported in AD, which supports the hypothesis of a relative derangement of the macrophage function in presenile AD patients.

Acute-Phase Proteins↗
PubMed1986

Therapeutic effect of lisuride in advanced Parkinson's disease.

The therapeutic effects of lisuride hydrogen maleate, a central dopamine agonist, were examined in 15 patients with advanced Parkinson's disease no longer satisfactorily responding to levodopa. A significant improvement (p less than 0.01) in the total Parkinson's disease disability score was obtained by the addition of lisuride to levodopa therapy. The clinical assessment in the follow-up was performed with 2 different disability scales that yielded a more precise evaluation of the efficacy of lisuride, an efficacy that, as with other dopaminergic drugs, showed a slight decrease in time after a mean of 3 months. No important adverse effects were noticed. The only limitation of the use of lisuride was the occurrence of reversible psychic disturbances. It is concluded from this study that lisuride is a valuable tool in the management of advanced Parkinson's disease that allows for a reduction of the side effects of levodopa therapy in the long-term treatment of the disease.

Aged↗
PubMedDate not supplied

Macrophage-colony stimulating factor (M-CSF) in the cerebrospinal fluid.

In a series of 145 cases with neurological diseases, macrophage-colony stimulating factor (M-CSF) was detected in cerebrospinal fluid of patients with brain tumors, bacterial meningitis, and less frequently, AIDS-dementia complex. Granulocyte-colony stimulating factor (G-CSF) was found only in patients with bacterial meningitis; granulocyte-macrophage (GM)-CSF was never detected. These findings suggest that M-CSF may play an important intrathecal immunoregulatory role in neoplastic and infectious diseases of the central nervous system.

Animals↗
PubMedDate not supplied

Occult small cell lung cancer associated with paraneoplastic neurologic syndrome: case report.

Cancer is often associated with paraneoplastic syndromes, which may be misinterpreted. We report a case of a patient with occult small cell lung cancer that was initially compounded by clinical features of a paraneoplastic neurologic syndrome. The presence of antineuronal antibodies and positron emission tomography scan guided the search for the underlying tumor. Following chemo-radiotherapy the patient showed no evidence of disease for the next 18 months, whereas only a slight improvement in the neurologic disorders was observed. The course of the small cell lung cancer was very indolent and the paraneoplastic neurologic syndrome did not worsen with the use of cisplatin.

Ataxia↗
PubMedDate not supplied

Immunological features of neurological paraneoplastic syndromes.

Neurological paraneoplastic syndromes are a rare group of disorders that occur in 1-2% of people with malignancy. They are usually caused by an immune response, triggered by and directed against a tumour, that cross-reacts with protein expressed by the peripheral or central nervous system. Any part of the nervous system can be affected and patients often develop severe and permanent disability. Diagnosis can be difficult as in two-thirds of patients the neurological problems appear up to 5 years before the tumour manifests. However, certain of these syndromes are often associated with specific serum autoantibodies that can be useful both in diagnosis of the neurological syndrome and in focusing the search for a particular tumour. Thus, these antibodies can allow earlier identification and treatment of cancer and, potentially, a reduction in morbidity and mortality. It was only in the 1980s that the first anti-neuronal autoantibodies were characterized and their associations with clinical syndromes and tumours defined. Further antibodies have been isolated over the past 20 years and novel pathogenic mechanisms for several syndromes have been recognized. For example, voltage-gate ion channels seem to be a common target for autoantibodies involved in peripheral nerve diseases such as the Lambert-Eaton myasthenic syndrome and neuromyotonia (Isaacs' syndrome). However, the place of most paraneoplastic antibodies in the pathogenesis of central syndromes is yet to be fully elucidated.

Central Nervous System Diseases↗