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Biomedical subjects

W Sheremata

Publications and source records attributed to W Sheremata.

34 records · Page 2Linked to original sources
PubMed1977

Studies of cellular sensitization to myelin antigens in multiple sclerosis. Dissociation of MIF and LBT production in response to a peptide encephalitogenic in rhesus monkeys.

The macrophage migration inhibitory factor (MIF) assay and the lymphoblastic transformation (LBT) technique were utilized simultaneously to measure immune responses to peptide Y, the 17 amino acid C-terminal fragment of basic myelin protein, in patients with multiple sclerosis (MS). Ten normals and 67 MS patients from the Montreal Neurological Hospital and affiliated institutions were examined. A prospective attempt was made to correlate the measured responses with phasic clinical activity of the disease. The LBT results indicate some degree of cellular sensitization to peptide Y which parallels the clinical course of the illness, and resembles earlier positive findings obtained with the whole basic myelin protein molecule. These findings, however, are in contrast to a negative MIF response to the Y peptide used in the present study and further contrast the positive MIF results obtained earlier using the whole protein. It is not evident from the results of the present study whether sensitization may be of any pathogenetic significance, but the findings show that differing portions of the basic myelin protein molecule may selectively stimulate specific lymphokine elaboration by sensitized lymphocytes.

Acute Disease↗
PubMed1977

Multiple sclerosis: sensitization of a myelin basic protein fragment (peptide T) encephalitogenic to primates. A preliminary report.

Myelin basic A1 protein is the sole antigen of the central nervous system capable of inducing experimental allergic encephalitis (EAE), but sensitization with peptide fragments of the molecule may also induce disease. Using the macrophage migration inhibition factor (MIF) assay we have compared sensitization to portions of the molecule active in inducing EAE in monkeys with results obtained concomitantly using the intact protein. Cellular sensitization to human myelin A1 protein, peptide L (residues 1-116), peptide T (residues 117-170), and petide Y (residues 154-170) was studied using the Thor-Rocklin MIF assay system. Lymphocytes of 10 normal subjects, 10 multiple sclerosis patients 0-3 weeks after onset, 10 4 weeks to 3 months after and 10 6 months or longer after onset of an acute exacerbation were assayed. Results of the investigation reveal evidence of cellular sensitization to myelin basic protein encephalitogenic peptide T occurring during attacks of multiple sclerosis. Peptide L, relatively nonencephalitogenic to primates, failed to induce a significant lymphocyte response, whereas peptide Y which is encephalitogenic gave irregular results.

Adult↗
PubMed1977

Cellular hypersensitivity in attacks of multiple sclerosis. I. A comparative study of migration inhibitory factor production and lymphoblastic transformation in response to myelin basic protein in multiple sclerosis.

Although cell-mediated hypersensitivity to basic myelin protein has been demonstrated in multiple sclerosis with use of cell migration assays, results with the lymphoblastic transformation technique have been inconclusive. However, prospective studies relating results of lymphoblastic transformation to the clinical course of multiple sclerosis have not been reported. In the present study, both lymphoblastic transformation and migration inhibitory factor assays were used, and results related to the temporal course of multiple sclerosis. Results of the present investigation show that cell-mediated hypersensitivity to myelin basic A1 protein is most significant during exacerbations of multiple sclerosis. Responses obtained employing either the lymphoblastic transformation or migration inhibitory factor assay were equally significant. The results support the hypothesis that a factor suppressing deoxyribonucleic acid synthesis is present in multiple sclerosis and is inhibited by the use of steroids.

Cell Migration Inhibition↗
PubMed1977

Retrobulbar neuritis. In vitro evidence of sensitization to myelin basic protein in patients without multiple sclerosis.

Thirty-six normal subjects and 34 patients with retrobulbar neuritis were studied with use of the technique of macrophage migration inhibition factor assay and myelin basic protein as antigen. Serial studies were carried out when possible. Normal subjects gave a mean migration index of 100.9+/-9. Eleven patients with retrobulbar neuritis alone gave a mean migration index of 55+/-16 in the first 3 weeks of illness, 89+/-17.3 during the fourth to the twenty-fourth weeks, and 100.9+/-9.0 after the twenty-fourth week. Ten multiple sclerosis patients with retrobulbar neuritis gave values of 61+/-21 in the first 3 weeks of an attack and 92+/-22.8 during the fourth to the twenty-fourth weeks, and 12 other multiple sclerosis patients 24 weeks or longer after an attack gave a value of 101.9+/-12.6. In a mean follow-up period of 1.9 years, only two patients presenting with retrobulbar neuritis alone have had a diagnosis of multiple sclerosis established; three others have weakness and reflex change in one limb only; and four have minor psychiatric problems. One retrobulbar neuritis patient has a family history of multiple sclerosis, but has no neurologic abnormalities. Comparison of these studies in both groups shows no statistical differences and supports the concept that cell-mediated hypersensitization to central nervous system myelin basic protein, however initiated, is a factor in the pathogenesis of retrobulbar neuritis.

Cell Migration Inhibition↗
PubMed1976

Multiple sclerosis and cell-mediated hypersensitivity to myelin A1 protein.

Cellular hypersensitivity to myelin basic (A1) protein was evaluated using the MIF assay in 246 subjects. Of 100 with multiple sclerosis positive results are seen in relationship to acute exacerbations of illness. Normal control subjects gave a mean value of 100 +/- 9% whereas patients studied within 4 weeks of onset of illness gave a result of 59 +/- 12.5%. A convalescent group studied between 5 and 12 weeks after an attack gave results of 86 +/- 22.2%. A chronic group gave a mean of 91 +/- 8.2%. Positive values were also seen in a number of other patients with central or peripheral nervous system disease especially those with "autoimmune disease". However, results of this study clearly establish a temporal relationship between in vitro evidence of hypersensitivity to A1 protein and clinical expression of disease.

Acute Disease↗
PubMed1976

Cerebrospinal fluid T and B lymphocyte kinetics related to exacerbations of multiple sclerosis.

Cerebrospinal fluid T and B lymphocyte populations were identified in 21 patients with relapsing and 10 patients with stable multiple sclerosis. The results indicate that the percentage of T cell is largest in the acute stage of a relapse (65 percent) and diminishes by the second week (41 percent). Conversely, the stable patients had a lower percentage of T cells (30 percent) and a relatively high percentage of nonreacting cells (66 percent). The proportion of T cells in the cerebrospinal fluid varies directly with the clinical activity of the disorder, further implicating cellular immune mechanisms in the pathogenesis of multiple sclerosis.

Adult↗
PubMed1975

Cellular hypersensitivity to basic myelin (P2) protein in the Guillain-Barré syndrome.

Lymphocytes of 29 subjects were assayed for MIF production in response to P2 peripheral nerve protein, crude human peripheral nerve and human central nervous system Al basic myelin protein. Seven were performed in normal control subjects, 12 in Guillain-Barre patients (GB), 5 with other polyneuropathies and 5 in patients with multiple sclerosis (MS). Only GB patients with acute illness produced MIF in response to neuritogenic P2 protein and crude human nerve. Two MS patients in the acute phase of an exacerbation and one GB patient produced MIF in Response to Al protein. The results of this study demonstrate cellular hypersensitivity to a neuritogenic consituent in peripheral nervous tissue and support the concept that this may be important in the pathogenesis of GB.

Adolescent↗
PubMed1975

Cellular hypersensitization to peripheral nervous antigens in the Guillain-Barré syndrome.

The macrophage migration inhibition factor assay was used as a specific measure of cellular hypersensitivity to peripheral nervous system antigen in a large group of Guillain-Barre patients and control subjects. Lymphocytes from 34 patients with Guillain-Barre syndrome, 33 with other peripheral nervous system disease, and 33 normal controls were assayed for production of macrophage migration inhibition factor. A mean of 101 +/- 7.2 was obtained in the control group, 70 +/- 16.3 in the Guillain-Barre syndrome group, and 96 +/- 11.3 in those with other peripheral nervous system disease. Twenty-six of the 34 patients with Guillain-Barre syndrome, two patients with myeloradiculitis, and two with Bell's palsy gave significant values. These results support the hypothesis that cellular hypersensitization to peripheral nervous system antigens is a pathogenetic factor in Guillain-Barre syndrome.

Antigens↗
PubMedDate not supplied

Natural alpha interferon in multiple sclerosis: results of three preliminary series.

In three preliminary, sequential series conducted between 1987-1991, natural human leukocyte interferon-alpha [HuIFN(Le)] was evaluated in 49 interferon-naive multiple sclerosis (MS) patients. In this study, safety data are reported for all 49 patients, and efficacy data for 45 of 49, each patient having received 3-12 months of therapy during the initial study year with observation only in the second year. No major side-effects for HuIFN(Le) were observed at doses of 5-30 million international units (MIU) per week for 3-12 months, although severe fatigue caused some patient drop-outs prior to completion of 3 months of therapy. The relapse rate in patients having received HuIFN(Le), prospectively evaluated in two series (34 patients), was reduced by 80% at 2 years. An unexpected trend towards improved disability provoked a retrospective analysis. In the first year, 36 of 45 (80%) patients improved or stabilized (P = 0.0001); of these 26 of 45 (58%) improved and 10 of 45 (22%) stabilized (P = 0.0023, chi 2 = 9.3). In year 2, 34 of 45 (76%) were improved/stabilized (P = 0.001); of these, 24 of 45 (53%) remained improved and 10 of 45 (22%) remained stable (P = 0.01, chi 2 = 6.6). A trend to greater efficacy at the higher doses for longer periods of therapy, up to 12 months, was observed.

Adolescent↗