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Biomedical subjects

W M Behan

Publications and source records attributed to W M Behan.

At least 55 records · Page 3Linked to original sources
PubMed1987

The inflammatory process in polymyositis: monoclonal antibody analysis of muscle and peripheral blood immunoregulatory lymphocytes.

An analysis was made of the lymphocyte subpopulations in the muscle lesions and the peripheral blood of 25 patients with inflammatory myopathy, in the acute or chronic phase of the disease. Percentages of activated T lymphocytes (65% +/- 3.4), both helper and suppressor/cytotoxic, macrophages (25% +/- 3.2) and B cells (11% +/- 0.9) in the tissues were similar at all stages of the illness; T cells were, however, more common in acute polymyositis than in acute dermatomyositis, where B cells were significantly increased. A loss of circulating OKT8-positive lymphocytes in the peripheral blood was demonstrated, supporting other evidence of disturbed immunoregulation. It was concluded that the attack on muscle fibres is mediated by T cells, macrophages, and B cells, with the first two playing the major roles.

Adolescent↗
PubMed1987

Experimental autoimmune thyroiditis: attempt to correlate disease development with lymphocyte subset changes.

An attempt was made to correlate lymphocyte subset abnormalities with the development of experimental autoimmune thyroiditis (EAIT) in thymectomized and irradiated rats of five inbred strains. The peripheral blood subpopulations were analysed using the fluorescence-activated cell sorter (FACS-IV). A significant lymphopenia with a severe decrease in helper T cells was identified in all the treated rats. In addition, a significant loss of suppressor cytotoxic T cells was found in rats of the most susceptible strain (August) and in the majority of affected individual rats of the other strains. The simple, modified protocol which we used revealed differences in strain susceptibility to EAIT, with 66% of August rats having histological evidence of disease, 50% of Lewis, 44% of Agus, 30% of Hooded Lister and 20% of Wistar, at 5 to 8 months after treatment. Levels of antithyroglobulin antibody, estimated by an ELISA assay, correlated well with the histological results. In all groups, three times as many females as males were affected. Our findings support the view that genetic and immunoregulatory factors are involved in the development of EAIT, with loss of both helper and suppressor cells playing an important role.

Animals↗
PubMed1986

Similarities between the Forssman carotid syndrome and experimental allergic encephalomyelitis.

The Forssman carotid syndrome was induced in guinea pigs to study the mechanism of demyelination-like lesions in this animal model and to compare it with experimental allergic encephalomyelitis days after intracarotid injection of rabbit anti-Forssman antibody and chronic lesions at 7-21 days post injection, using routine histological, immunofluorescent, and electron-microscopic techniques. The results were compared to those in a group of guinea pigs with acute or chronic lesions of EAE. The picture was remarkably similar in the two conditions, in regard to localization in the central nervous system (CNS), composition of cellular infiltrates, diameter of lesions produced, myelin loss and axonal degeneration, together with gamma globulin deposition in small vessels in affected areas. The differences were that in the Forssman carotid syndrome, in contrast to EAE, there were no mononuclear cell infiltrates in the acute phase, and no evidence of macrophages invading myelin sheaths was detected. Perivascular lesions consisted of demyelination within infiltrates of mono-nuclear cell in chronic relapsing EAE, but not in the Forssman carotid syndrome. It is suggested that investigation of the CNS may be of benefit in the pathogenetic study of demyelinating disease.

Acute Disease↗
PubMed1986

Anti-endothelial cell antibody and immune complexes in the sera of animals with acute experimental allergic encephalomyelitis and chronic relapsing experimental allergic encephalomyelitis.

Blood-brain barrier (BBB) injury occurs in both acute and chronic relapsing experimental allergic encephalomyelitis (EAE). Sera from animals in which these forms of EAE had been induced were examined for anti-endothelial cell antibodies and immune complexes by enzyme-linked immunosorbent assay (ELISA) using either cultured endothelial cells or Raji cells. IgG binding to endothelial cells was significantly increased in the sera of animals with acute EAE and chronic relapsing EAE, compared to controls. Increased levels of circulating immune complexes were also detected in the sera of some animals with chronic relapsing EAE, especially those in an exacerbation. It is suggested that the anti-endothelial cell antibody and immune complexes detected may play pathogenetic roles in the destruction of the BBB in EAE.

Animals↗
PubMed1986

Lymphocyte subset abnormalities in patients with spasmodic torticollis.

The aetiology of spasmodic torticollis is unknown but the patients form a heterogeneous group among which are cases apparently precipitated by a viral illness and others associated with autoimmune disease. We therefore decided to investigate the immunoregulatory lymphocyte subsets in our 11 cases. A significant decrease of both helper and suppressor lymphocytes was identified in the group, together with in vitro evidence of depressed suppressor cell function. Disturbance of the immune response may play a role in this puzzling disorder.

Adult↗
PubMed1986

Pathogenesis of heart block in a fatal case of dermatomyositis.

Approximately 70% of patients with dermatomyositis have evidence of cardiac damage; in one third of cases this affects principally or solely the conduction tissue. In infants similar histological lesions have been associated with a maternal autoantibody, anti-Ro, that crosses the placenta and produces congenital heart block. Anti-Ro antibody was detected in a fatal case of dermatomyositis with lesions of the conduction system.

Atrioventricular Node↗
PubMed1985

Search for autoantibodies to endothelial and smooth muscle cells in patients with multiple sclerosis.

The blood-brain barrier (BBB) is disrupted in many of the lesions of multiple sclerosis (MS). Immunologically mediated injury to one of the major components of this barrier, the cerebral capillary, may play a role in the development of the lesion. We therefore examined the sera of 51 cases of MS for the presence of autoantibodies to endothelial and smooth muscle cells, using the indirect immunofluorescent technique. The results were compared to those in other groups of patients with neuroimmunological disorders. We found no anti-endothelial cell antibodies, but autoantibodies to vascular smooth muscle were detectable in 31% of the MS sera tested. They were also present, however, in 30% of sera from cases of myasthenia gravis and in the serum of one of 12 cases of polymyositis. It is considered to be unlikely that antibodies to vascular tissues play any pathogenetic role in multiple sclerosis.

Antibodies, Antinuclear↗
PubMed1985

The postviral fatigue syndrome--an analysis of the findings in 50 cases.

The clinical, pathological, electrophysiological, immunological and virological abnormalities in 50 patients with the postviral fatigue syndrome are recorded. These findings confirm the organic nature of the disease. A metabolic disorder, caused by persistent virus infection and associated with defective immunoregulation, is suggested as the pathogenetic mechanism.

Adolescent↗
PubMed1984

Recent advances in polymyositis.

The most typical clinical features of polymyositis (PM), the criteria of diagnosis and principles of treatment are outlined. An inflammatory disease of muscle, PM also frequently affects other organs such as the skin and hence the name dermatomyositis. The principal cardiac symptom is a peculiar disturbance of atrioventricular conduction, correlated with a specific anti-Ro autoantibody, present in 25% of patients. The etiology of PM is as yet unknown, although there is evidence for an autoimmune pathogenesis. It is frequently found in association with other immune-mediated diseases such as myasthenia gravis, pemphigus, immune-complex vasculitis and Sjogren syndrome. Laboratory investigations show hypergammaglobulinemia, a decrease of complement factors C3 and C4 and the presence of circulating immune complexes in 70% of patients. Very frequent, especially in cases of dermatomyositis, is a histologically detectable accumulation of IgG and complement in the walls of the intramuscular venous vessels. Cell-mediated hypersensitivity, emphasised formerly as highly significant in PM, has not been confirmed. The presence of specific antimyoglobin lymphocyto-toxicity, once considered to be the hallmark of muscle degeneration in PM, has been excluded by a number of laboratories. In a personal series of patients with various clinical forms of PM a severe loss of suppressor/cytotoxic lymphocytes was found in the peripheral blood and a relative increase in the first subset. These results support the hypothesis that a serious disturbance of immunoregulation is present in PM and is the cause of a multitude of immunological anomalies, the characterisation of which is under study.

Adrenal Cortex Hormones↗
PubMed1983

Does Toxoplasma cause polymyositis? Report of a case of polymyositis associated with toxoplasmosis and a critical review of the literature.

We report here a case of polymyositis and toxoplasmosis, and review the previous examples of this association. We suggest that in most cases this relationship is due to reactivation of latent infection in an immunocompromised host. Gross immunological aberrations underline the pathogenesis of polymyositis and these predispose the patient to the development of toxoplasmosis. Anti-protozoal therapy is necessary and produces some clinical benefit, but it does not cure the polymyositis.

Adult↗