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Biomedical subjects

R P Lisak

Publications and source records attributed to R P Lisak.

At least 19 recordsLinked to original sources
PubMed1992

A combination of adoptive transfer and antigenic challenge induces consistent murine experimental autoimmune encephalomyelitis in C57BL/6 mice and other reputed resistant strains.

Adoptive EAE was induced in SJL mice by the transfer of MBP-primed and in vitro-stimulated donor lymph node cells into naive syngeneic recipients. Priming donor mice with OVA instead of restimulating MBP-primed donor cell with OVA resulted in no transfer of EAE. This apparent lack of disease, however, could be overcome if the recipients were subsequently challenged with MBP. When this transfer-challenge technique was applied to BALB/c and C57BL/6 mice, these reputed (MBP)EAE-resistant strains developed consistent and severe disease similar to that seen in susceptible strains. In fact, a survey of eleven (MBP)EAE-resistant strains, defined on the basis of their inability to mount an encephalitogenic response in recipient mice following the transfer of MBP-primed and in vitro activated lymph node cells, revealed that EAE could be induced in all these strains. Since the surveyed strains represented a wide spectrum of genetic backgrounds as well as the common MHC congenic haplotypes (H-2b,d,k,m,r,s,v), it is concluded that the machinery for recognition of MBP, i.e. MHC genes and the appropriate T cell receptors, is functionally intact in these resistant mice. While MHC and T cell receptor genes are required for T cell responses, they are not the limiting factors that confer resistance in murine EAE.

Animals↗
PubMed1992

Differences in the capacity of gamma-interferons from different species to induce class I and II major histocompatibility complex antigens on neonatal rat Schwann cells in vitro.

We compared the capacity of unfractionated cytokines and recombinant gamma-interferons (gamma-IFN) to induce major histocompatibility (MHC) antigens on neonatal rat Schwann cells and endoneurial fibroblasts in vitro. Rat and mouse gamma-IFN were capable of induction of both class I and class II MHC antigens on both cell types although rat gamma-IFN was more potent than that of mouse. Human gamma-IFN failed to induce MHC class I or class II on either cell type. Unfractionated cytokines from the different species also differed in their capacity to induce MHC antigens. Differences in species of origin of cytokine mixtures as well as in individual cytokines, such as gamma-IFN need to be considered in studies of MHC induction. The presence of MHC class I and class II antigens on Schwann cells could render them susceptible to cytotoxic reactions and allow for the presentation of antigen, respectively.

Animals↗
PubMed1992

Effect of clinical status and treatment on the frequency of CD5+ B cells in patients with myasthenia gravis.

CD5+ B cells comprise a subset of B lymphocytes that may play a pathogenetic role in the development of human autoimmune disease. We previously reported a high-frequency phenotype (greater than 30% CD5+ B cells) in the peripheral blood of 57% of myasthenia gravis (MG) patients and 13% of controls. We have now examined additional patients (n = 41) and controls (n = 27) and continue to find that 44% of MG patients have a high-frequency phenotype of CD5+ B cells compared with 7% of controls. Serial studies showed that the frequency of CD5+ B cells in peripheral blood remained fairly stable for controls and that it may decrease with immunosuppressive therapy of MG patients. In patients receiving anticholinesterase only or no therapy (n = 21), the age at onset of MG, presence or absence of detectable serum anti-acetylcholine receptor antibody, clinical extent of MG, and the duration of disease may affect the frequency of CD5+ B cells in the blood.

Adult↗
PubMed1991

Antibodies to interleukin-1 inhibit cytokine-induced proliferation of neonatal rat Schwann cells in vitro.

Unfractionated cytokines have been shown to induce in vitro proliferation of neonatal rat Schwann cells but the nature of the mitogen(s) is not known. A mixture of rabbit antibodies specific for recombinant interleukin-1 alpha (IL-1 alpha) and interleukin-1 beta (IL-1 beta) inhibited Schwann cell proliferation induced by unfractionated human cytokines whereas antibodies to interleukin-2 (IL-2) and control IgG did not. However, purified human IL-1 and recombinant human IL-1 alpha or beta did not induce Schwann cell proliferation on their own.

Animals↗
PubMed1990

Pokeweed mitogen-induced immunoglobulin secretory responses of thymic B cells in myasthenia gravis: selective secretion of IgG versus IgM cannot be explained by helper functions of thymic T cells.

The thymus, with its striking B cell infiltrates, is widely regarded as an important element in the pathogenesis of myasthenia gravis (MG) but its role remains to be elucidated. To gain further insight into the functional properties of MG thymic B cells, we studied the heavy chain isotype of immunoglobulin they produced in vitro in response to the T cell-dependent polyclonal activator pokeweed mitogen (PWM). MG thymic cells secreted prominent amounts of IgG but little IgM. In contrast, peripheral blood mononuclear cells (PBM) of the same subjects secreted similar amounts of IgG and IgM as did PBM of control subjects. In cell admixture experiments, MG thymic T cells, like PBM T cells, helped autologous PBM B cells produce IgM as well as IgG, although the overall magnitude of help for both isotypes appeared less than that of PBM T cells. Thus, in response to PWM, MG thymic B cells are largely committed to an IgG response and this likely reflects the intrinsic properties of these cells rather than the immunoregulatory properties of thymic T cells. This IgG isotype switch likely reflects in vivo activation events.

Adult↗
PubMed1990

The frequency of CD5+ B lymphocytes in the peripheral blood of patients with myasthenia gravis.

A subset of human B lymphocytes expresses Leu-1 (CD5), a pan-T cell marker, which is the equivalent of the murine Lyt-1 molecule. CD5+ B cells produce autoantibodies in vitro; therefore, they may play a role in the pathogenesis of autoimmune disorders. In myasthenia gravis (MG), autoantibodies are directed against the nicotinic acetylcholine receptor (AChR) at the neuromuscular junction. We examined the peripheral blood leukocytes of MG patients (n = 21) and controls (n = 15) for the presence of Leu-1+ B lymphocytes. A fraction of B-1 (CD20)+ cells expressed Leu-1 at a low density. There was a statistically significant difference in the frequency of Leu-1+ B cells between patients and controls. We observed 2 frequency ranges of Leu-1+ B cells (0 to 30% and above 30%), which were not related to the total percentage of B-1+ cells in the blood. Fifty-seven percent of MG patients had a high frequency of Leu-1+ B cells compared with 13% of controls.

Adult↗
PubMed1979

Experimental allergic neuritis induced by sensitization with galactocerebroside.

Thirteen of 31 rabbits immunized repeatedly with bovine brain galactocerebroside developed experimental allergic neuritis, manifested by flaccid paresis and hypesthesia of four limbs, 2 to 11 months after the initial inoculation. Electrophysiological studies revealed multifocal conduction block of peripheral nerves. Perivenular demyelinative lesions associated with phagocytic mononuclear cells occurred in spinal ganglia, roots, and less frequently in distal nerves.

Animals↗
PubMed1979

Cranial computed tomography in the diagnosis of systemic lupus erythematosus.

The cranial computed tomograms of 29 patients with systemic lupus erythematosus (SLE) were reviewed. Twenty-two patients had a clinical course consistent with central nervous system involvement. Of these, 20 had abnormal CT studies during the course of their CNS symptoms. The most common finding was sulcal enlargement, either with or without ventricular enlargement, and it was prominent in patients with either psychosis or dementia. Infarcts and intracranial hemorrhages were seen as well. Seven CT studies were obtained in SLE patients without a clear diagnosis of CNS involvement. Only one of these was abnormal.

Adolescent↗
PubMed1979

Antibodies to galactocerebroside bind to oligodendroglia in suspension culture.

Antisera raised in rabbits against galactocerebroside bind to bovine oligodendroglia in suspension in significant titer as demonstrated by indirect immunofluorescence. Absorption of antigalactocerebroside antiserum with galactocerebroside, oligodendroglia, or myelin markedly reduces the antigalactocerebroside antibody titer as measured by a radioimmunoprecipitation test as well as the binding to oligodendroglia. Incubation with some other galactose-containing glycolipids results in a parallel decrease in binding to oligodendroglia and reduction in antigalactocerebroside antibody titer. Antigalactocerebroside antibodies provide a useful and specific tool with which to study development of oligodendroglia and myelin as well as immunopathologic mechanisms which might be involved in demyelinating diseases.

Animals↗
PubMed1979

Immune response to isolated oligodendrocytes.

Oligodendrocytes were isolated from bovine white matter and were injected with complete Freund's adjuvant (CFA) into experimental animals. Indirect immunofluorescence studies using fluoresceinated goat anti-rabbit or anti-guinea pig immunoglobulin (GARIg; GAGPIg) showed that rabbit and guinea pig anti-oligodendrocyte (RAO, GPAO) sera reacted specifically with the surface of isolated oligodendrocytes in suspension, as well as with oligodendroglia in bovine and human brain sections, and in mouse cerebellum cultures. This activity of RAO was blocked by non-fluoresceinated GARIg and by GPAO, and absorbed by oligodendrocyte preparation (OP) or whole white matter, but not by purified myelin, neuroblastoma or non-brain tissue. Low levels of anti-basic protein antibodies were found in many RAO (but not GPAO) sera by radioimmunoassay, and a few showed significant anti-galactocerebroside antibody by agglutination and radioimmunoprecipation techniques. Guinea pigs sensitized with isolated oligodendrocytes in CFA showed cell-mediated immunity (CMI) to OP as manifested by delayed type skin test and induced in vitro lymphocyte transformation. CMI to purified myelin basic protein was not detected. The demonstration of humoral and CMI to the cell responsible for the production of CNS myelin may be related to some aspects of the immunopathogenesis of demyelinating disorders.

Animals↗
PubMed1979

A search for antibodies against glial cells in the serum and cerebrospinal fluid of patients with multiple sclerosis and Guillain-Barré syndrome.

We have used indirect immunofluorescence to examine the binding of immunoglobulin in sera from patients with multiple sclerosis, Guillain-Barré syndrome, other neurological diseases, and normal subjects to marker-identified glial cells in dissociated primary cell cultures of neonatal rat corpus callosum and sciatic nerve. In corpus callosum cultures all the sera tested showed weak surface staining of oligodendrocytes and of a small percentage of astrocytes and bright staining of fibroblasts. The cerebrospinal fluid from one patient with multiple sclerosis showed the same pattern of staining while the cerebrospinal fluid from other patients with multiple sclerosis and pathological controls only showed weak staining of fibroblasts. None of the sera stained the cytoplasm of oligodendrocytes in frozen sections of adult rat optic nerve. In sciatic nerve cultures all sera showed weak staining of Schwann cells and fibroblasts. Thus we were unable to distinguish patients with demyelinating diseases from normal individuals or from patients with other neurological diseases in terms of serum or cerebrospinal fluid anti-glial cell antibodies.

Autoantibodies↗
PubMed1979

Cold reactive antilymphocyte antibodies in neurological diseases.

Cold reactive (15 degrees C) antilymphocyte antibodies were detected in the sera of 33% of patients with multiple sclerosis, 50% with Guillain-Barré syndrome, 42% with myasthenia gravis, and 38% with polymyositis. We did not detect such antibodies against autologous cells in multiple sclerosis. In multiple sclerosis there was no correlation between the presence of antilymphocytic antibodies and disease activity or duration. In patients with multiple sclerosis, myasthenia gravis, and polymyositis there was no correlation between the presence of cold reactive antilymphocyte antibodies and abnormalities of T or B cell levels.

Antilymphocyte Serum↗