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S L Hauser

Publications and source records attributed to S L Hauser.

121 records · Page 7Linked to original sources
PubMed1983

Epinephrine-induced changes in the distribution of lymphocyte subsets in peripheral blood of humans.

We have previously demonstrated that mitogen responsiveness of mononuclear cells (MNC) from peripheral blood is reduced after a single injection of epinephrine to human subjects. The purpose of the present study was to characterize the relative distributions of MNC subsets after epinephrine administration using monoclonal antibodies and conventional cell markers. The absolute number of circulating MNC increased 64% within 30 min after injection of epinephrine, and returned to baseline by 2 hr. Analysis of MNC subsets revealed that there were no changes in the relative percentages of total T lymphocytes [T3+ cells, or neuraminidase-treated sheep red blood cell rosettes (EN-rosettes)], B lymphocytes (B1+, or cells with surface-bound immunoglobulin), or monocytes (by morphologic criteria) after epinephrine administration. The percentage of inducer T cells (T4+) declined at 30 and 60 min postinjection. Overall, the percentage of suppressor/cytotoxic T cells (T8+) did not change after injection of epinephrine; however, analysis of individual subjects revealed opposing responses of this subset. The T4:T8 ratio was 2.19 before injection, declined to 1.56 at 60 min, then increased to 3.10 2 hr postinjection. The percentage of natural killer/killer cells (HNK-1+) increased from a baseline of 15.5% before epinephrine injection to 29.6% at 30 min postinjection, then declined to 11.4% at 2 hr. Therefore, the administration of physiologic doses of epinephrine results in changes in the relative proportions of lymphocyte subsets in peripheral blood, in addition to reduced mitogen responsiveness as reported previously.

B-Lymphocytes↗
PubMed1982

Clonally restricted B cells in peripheral blood of multiple sclerosis patients: kappa/lambda staining patterns.

The presence of clonally restricted B lymphocytes in the peripheral blood of patients with multiple sclerosis (MS) was investigated using a cytofluorometric technique able to detect lymphocytes having homogeneous amounts of surface immunoglobulin of one light chain class. Thirty-five of 76 analyses (46%) performed on 63 MS patients were positive for increased numbers of clonally restricted B cells as compared with only 7 of 27 (26%) in patients with other neurological diseases (p less than 0.05) and 9 of 36 (25%) in control subjects (p less than 0.05). This B cell population expressed predominantly kappa light chain determinants in 16 of 18 MS patients (89%) but in only 6 of 11 (55%) controls (p less than 0.005). There was no correlation between the presence of abnormal B cell clones in peripheral blood and either disease activity or serum antimeasles antibody titers. The results demonstrate that there are increased numbers of clonally restricted B cells in the peripheral blood of MS patients which may be related to the oligoclonal immunoglobulin found in the serum and cerebrospinal fluid.

B-Lymphocytes↗
PubMed1982

Neuroimmunology I: Immunoregulation in neurological disease.

Aberrations in immune function that ultimately result in disease states may involve three aspects of immune regulation: (1) regulatory T cells, which both suppress and induce immune responses; (2) idiotype-antiidiotype networks, which serve as internal regulatory networks during generation of an immune response; and (3) immune response genes, which determine genetic differences in an individual's immune response. Three major diseases of the nervous system, multiple sclerosis, myasthenia gravis, and acute inflammatory polyneuropathy (Guillain-Barré syndrome), are classified as "autoimmune" in nature and may be due to underlying disorders of immunoregulation. In multiple sclerosis there is a loss of suppressor T cells in the peripheral blood during attacks, in myasthenia gravis there are thymic abnormalities and antibodies against the acetylcholine receptor, and in acute inflammatory polyneuropathy, macrophage-mediated destruction of peripheral nerve myelin occurs in the context of sensitized T cells and is usually associated with a preceding viral illness. In each of these diseases the following central questions must be answered: (1) against what antigen (or antigens) of the nervous system is the autoimmune response directed? (2) what is the mechanism of immune damage? and (3) what initiates, or triggers, the autoimmune response?

Antibodies, Monoclonal↗
PubMed1982

Childhood multiple sclerosis: clinical features and demonstration of changes in T cell subsets with disease activity.

Using monoclonal antibodies that identify T cell subsets in human beings (T4 = inducer cell; T5 = suppressor/cytotoxic cell), we have previously shown that most patients with multiple sclerosis (MS) have decreased T5 cells and an elevated T4:T5 ratio during periods of disease activity. We have recently studied three children with MS beginning at 4 years 11 months, 101/2 years, and 2 years 11 months of age. Clinical symptoms included a relapsing brainstem syndrome in the first, Devic syndrome and recurrent optic neuritis in the second, and multiple attacks with accumulating neurological deficits in the third. Two of these children represent the youngest cases of MS yet reported. In each child, circulating T5 cells were reduced or absent during an acute exacerbation of disease; following stabilization, T5 cells returned and the T4:T5 ratio became normal. No changes in T cell subsets were seen in a group of age-matched healthy children or in children suffering from other neurological diseases. Our finding that young children with active MS have a pattern of T cell abnormalities identical to that of adult MS patients suggests that the same pathophysiological process which causes MS in adults occurs in young children as well.

Antibodies, Monoclonal↗
PubMed1982

Neuroimmunology. II: Antigenic specificity of the nervous system.

Antigenic specificity of the nervous system refers to a property conveyed by unique cell surface structures that are present on different classes of nervous system tissue. These structures are of major importance for the study of nervous system structure and function, and can play a central role in determining patterns of nervous system injury. Thus, the major classes of nervous system cells are identified by structures that are unique to them: neurons by the presence of tetanus toxin receptors on their surface and oligodendrocytes by the presence of surface galactocerebroside, for example. With the advent of hybridoma technology, a large number of monoclonal antibodies are being identified which have increased by several orders of magnitude the ability to define subclasses of nervous system tissue according to unique antigens. In addition, surface antigens of nervous system tissue may determine the specificity of nervous system injury by (1) functioning as receptors for viruses or (2) being the targets of autoimmune responses. Patterns of viral injury to the nervous system are often extraordinarily selective (e.g., poliovirus tropism for motor neurons), and nervous system viral tropism is due is some instances to the interaction of a virus with a unique surface antigen on neural cells. The specificity of injury in autoimmune disease (such as that against the acetylcholine receptor in myasthenia gravis) likewise must be explained by an immune response against unique antigenic determinants on the tissue being damaged. Some antigens are known to be shared between nervous system and other tissues or between nervous system and infectious agents such as bacteria or viruses. The presence of shared antigenic structures between the nervous system and infectious agents creates the possibility that an immune response generated against a virus may concurrently damage normal nervous system tissue.

Antigens↗
PubMed1980

Loss of suppressor T cells in active multiple sclerosis. Analysis with monoclonal antibodies.

To determine whether abnormalities of immunoregulatory T cells are associated with multiple sclerosis (MS), we characterized peripheral lymphocytes in 33 patients with untreated MS and compared them with 42 normal persons and 29 age-matched control subjects who had other neurologic diseases. For this analysis, we used monoclonal antibodies to the surface antigens of helper (T4) and suppressor (T5) T-cell subsets and to a common T-cell antigen (T3). In contract to normal persons and the controls with other neurologic diseases, the patients with MS had a reduced percentage of T3-positive (T3+) cells (P less than 0.05). More importantly, there was a selective decrease in T5-positive (T5+) cells in 11 of 15 patients with active MS, but in only one of 18 patients with inactive MS and in none of the normal persons or controls with neurologic disease (P less than 0.00001). Serial analysis of five patients with MS showed a correlation between the absence of the T5+ subset and disease activity. Thus, there is loss of peripheral suppressor cells in many patients with active MS, suggesting that immunoregulatory abnormalities contribute to the pathogenesis of the disease.

Adolescent↗
PubMed1980

Autism and mental retardation: neuropathologic studies performed in four retarded persons with autistic behavior.

Four persons who exhibited prominent autistic features throughout life died when 4, 14, 27, and 33 years old. All were mentally retarded. One had documented phenylketonuria, but the cause of mental retardation and autistic behavior was undefined in three. At the time of autopsy, brain weights were within 2 SDs of the norm for age. Complete neuropathologic examination, including analysis of cortical neurons impregnated with the rapid Golgi method, failed to provide clues as to cause or the pathoanatomic substrate of autistic behavior in these cases.

Autistic Disorder↗
PubMed1979

Lymphocyte capping in muscular dystrophy.

We investigated lymphocyte capping in nine patients with muscular dystrophy (seven with Duchenne dystrophy and two with limb-girdle dystrophy), nine carriers, and five normal controls. No differences between the groups were observed. Thus, we have been unable to confirm a recent report that patients with muscular dystrophy, as well as carriers, have a defect in lymphocyte capping.

Animals↗
PubMed1975

Pneumographic findings in the infantile autism syndrome. A correlation with temporal lobe disease.

Pneumoencephalographic findings are described in a group of 18 children who presented to us with a history of retarded language development and autistic behaviour disturbances. None had specific diagnosable neurological diseases nor gross motor disorders. PEG findings included, most prominently, pathological enlargement of the left temporal horn in 15 cases; some cases showed enlargement of both temporal horns or mild variable enlargement of the lateral ventricles, especially the left. Comparisons between infantile autism and recognized patterns of temporal lobe disease (especially Korsakoff syndrome and Kluver-Bucy syndrome) are drawn. We have suggested that medial temporal lobe dysfunction may be a major factor in the pathogenesis of the syndrome of infantile autism.

Autistic Disorder↗
PubMedDate not supplied

Analysis of human T-lymphotrophic virus sequences in multiple sclerosis tissue.

Several observations suggest that retroviral infection is involved in the pathogenesis of the human demyelinating disease multiple sclerosis (MS). First, lymphadenopathy-associated virus/human T-lymphotropic virus type III (LAV/HTLV-III), the agent of acquired immune deficiency syndrome (AIDS), has been shown to be neurotropic in man. Second, the genetic organization of the lentivirus visna, which causes a chronic demyelinating disease of sheep, closely resembles that of LAV/HTLV-III. Recently, Koprowski and colleagues reported that MS is associated both with raised levels of circulating antibodies to HTLV-I and with the presence of HTLV-I-specific RNA within cell lines derived from the cerebrospinal fluid (CSF). Here we report that no HTLV-I-like or LAV/HTLV-III-like sequences can be detected, by in situ hybridization, in central nervous system (CNS) tissues from MS patients, and that nonspecific HTLV-I-like signal in peripheral blood mononuclear cells or in CSF cell lines is characteristic of MS. Furthermore, enzyme-linked immunosorbent assay (ELISA) analysis of circulating and CSF antibodies for HTLV-I reactivity fails to distinguish between MS and control groups.

Antibodies, Viral↗