Search PubMed⌕ Search

Biomedical subjects

L Steinman

Publications and source records attributed to L Steinman.

At least 253 records · Page 14Linked to original sources
PubMed1984

Homing of Lyt-2+ and Lyt-2- T cell subsets and B lymphocytes to the central nervous system of mice with acute experimental allergic encephalomyelitis.

Subpopulations of lymphoid cells were compared with respect to their ability to migrate into the central nervous system (CNS) of mice with acute experimental allergic encephalomyelitis (EAE). In mice with established lesions, the majority of cells homing to the CNS are not presensitized to CNS antigens. B cells had a much reduced capacity to migrate into the CNS of sick mice compared with T cells. However, T cells of both the Lyt-2+ and Lyt-2- subsets homed equally well to the CNS. The relative paucity of B cells in the lesions of EAE and multiple sclerosis may thus partly result from the limited ability of these cells to migrate into the CNS across the blood-brain endothelial barrier. The predominance of Lyt-2- T cells over Lyt-2+ cells in these CNS lesions is unlikely to result from such a difference in homing capacity, but may reflect the ratio of these two cell types in the blood or preferential in situ expansion of the Lyt-2- population.

Animals↗
PubMed1983

Anti I-A antibody suppresses active encephalomyelitis: treatment model for diseases linked to IR genes.

To test the clinical relevance of monoclonal anti-I-A antibody in autoimmune disease, we investigated the effects of such a therapy in acute and chronic relapsing experimental allergic encephalomyelitis (EAE) by instituting treatment after the onset of paralytic signs and following the clinical course. In chronic relapsing EAE, animals treated with anti-I-As antibody had no mortality and fewer relapses when compared with control animals. Antibody levels to myelin basic protein were lower and histopathology showed milder lesions in the treated group. Similarly, in the acute EAE model, animals treated with anti-I-As antibody showed a dramatic reversal of paralytic signs and a rapid recovery. The mechanisms of action of antibody to IR gene products in autoimmune disease are discussed.

Animals↗
PubMed1983

Administration of myelin basic protein-coupled spleen cells prevents experimental allergic encephalitis.

Intravenous administration of mouse myelin basic protein covalently coupled with chromic chloride to syngeneic spleen cells (MBP-SC) prevents the subsequent induction of experimental allergic encephalitis (EAE). Whereas 1 in 28 mice receiving MBP-SC developed EAE after immunization with mouse spinal cord homogenate (MSCH) and adjuvants, 16 out of 25 mice receiving ovalbumin-coupled spleen cells (OA-SC) had EAE following encephalitogenic challenge. The effect of administration of antigen-coupled spleen cells on in vitro proliferation responses is shown.

Animals↗
PubMed1983

Prevention of experimental allergic encephalitis with in vivo administration of anti I-A antibody. Decreased accumulation of radiolabelled lymph node cells in the central nervous system.

Experimental allergic encephalitis (EAE) can be prevented with the in vivo administration of monoclonal anti I-A antibody. A radiometric assay was developed to measure the accumulation of lymphocytes in the central nervous system of EAE animals. A direct correlation was observed between severity of clinical disease and the amount of radiolabelled lymph node cells (LNC) in the central nervous system. Injection of anti I-A antibody in vivo prevented clinical EAE and decreased the accumulation of radiolabelled LNC in spinal cord after immunization with mouse spinal cord homogenate and adjuvants.

Animals↗
PubMed1983

In vivo therapy with monoclonal anti-I-A antibody suppresses immune responses to acetylcholine receptor.

A monoclonal antibody to I-A gene products of the immune response gene complex attenuates both humoral and cellular responses to acetylcholine receptor and appears to suppress clinical manifestations of experimental autoimmune myasthenia gravis. This demonstrates that use of antibodies against immune response gene products that are associated with susceptibility to disease may be feasible for therapy in autoimmune conditions such as myasthenia gravis.

Animals↗
PubMed1983

The neuropathology of propionic acidemia.

The neuropathology in two biochemically documented cases of propionic acidemia is presented. While spongiform changes in white matter were seen in the infant who died at 12 days, no such changes were evident in an older patient who died at age 23 months. These findings are compared with other aminoacidemias.

Amino Acid Metabolism, Inborn Errors↗
PubMed1982

Identification of T cell subsets and B lymphocytes in mouse brain experimental allergic encephalitis lesions.

Tissue section immunoperoxidase staining, employing monoclonal antibodies specific for T cell antigens (Lyt-1, Lyt-2) and B cells (B220), was used to study the brains of mice with experimental allergic encephalitis. Cells bearing phenotypes characteristic of both helper (Lyt-1+2-) and cytotoxic/suppressor (or precursor) (Lyt-2+) T cells, as well as B cells, are present in the perivascular cuffs in brains of EAE mice during active disease and the recovery phase. Lyt-1+ cells comprise 49% of the inflammatory cell population, and Lyt-2+ and B220+ cells are found at frequencies of 10% and 12%, respectively.

Animals↗
PubMed1981

Specificity of antigen binding by T cells; competition between soluble and Ia-associated antigen.

Competitive antigen binding experiments were performed with purified T and B cells of C3H.SW (H-2b) mice. As antigen, (T,G)-A--L [poly-L(Tyr,Glu)-poly-DL-ALa-poly-L Lys] was used, both in an Ia-containing form, released by adherent cells (IAC-Puri and Lonai, Eur. J. Immunol. 1980. 10:273), and in regular solution. It was found that regular (T,G)-A-L did not compete with the binding of 125I-labeled-IAC-(T,G)-A--L even at a 10(4)-fold excess, whereas IAC-(T,G)-A--L inhibited binding at 10-fold excess. The specificity of (T,G)-A--L binding to high-responder T and B cells was compared by using related branched synthetic copolymers as competitors. B cells cross-reacted with (T,G)-A--L, (H,G)-A--L, (G)-A--L and (T,G)-Pro--L. In contrast, antigen binding C3H.SW T cells cross-reacted only with (T,G)-A--L and (Phe, G)-A--L to both of which they are Ir gene-controlled high responders. Evidence for the Ir gene control of IAC-binding T cells was obtained by showing that high X low responder F1 hybrid T cells preferentally bind IAC-(T,G)-A--L processed by processor cells deriving from the high-responder parental strain. These data are interpreted to suggest that T cells have high affinity for antigen plus self Ia complexes, whereas they have a much lower, if any, affinity for free antigen. It also follows from the results that the structure of the complex ligand may have a role in defining the specificity, H-2 restriction and Ir gene control of T cells.

Animals↗
PubMed1981

In vivo effects of antibodies to immune response gene products: prevention of experimental allergic encephalitis.

Prevention of experimental allergic encephalitis in SJL/J [H-2s] mice was achieved with in vivo administration of antibody reactive with I-As gene products prior to immunization with spinal cord antigen. No protection was evident in animals that received antisera specific for I-Js gene products. Administration of antibody to I-As beginning 5 days after immunization with spinal cord antigen delayed, but did not prevent, the onset of experimental allergic encephalitis.

Animals↗
PubMed1980

Isolated oculomotor palsy after measles immunization.

A 17-month-old healthy boy had a rapid onset of right oculomotor nerve palsy, and spontaneous recovery after measles immunization. Results of computed tomography scan, skull x-ray, chest x-ray, intravenous pyelogram, and bone marrow examination were all normal. Serum antibody titers showed effective measles immunization.

Blepharoptosis↗
PubMed1980

Natural occurrence of thymocytes that react with myelin basic protein.

In adult strain 13 guinea pigs, two lines of evidence show that there are natural autoreactive thymocytes that can react with myelin basic protein (BP) or the encephalitogenic nonapeptide (EP). An autoradiographic binding assay revealed antigen-specific receptors for 125I-BP on thymocytes. A 3H-thymidine antigen-specific proliferation assay demonstrated that normal thymocytes were activated by EP- or BP-pulsed macrophages. Soluble BP suppressed the activation of thymocytes by macrophage-associated BP. The mode of presentation of BP or EP, whether macrophage-associated or soluble, may be critical in maintaining self-tolerance and preventing an autoimmune attack on the central nervous system.

Animals↗
PubMed1979

Cherry-red spot-myoclonus syndrome.

A 21-year-old woman had typical clinical and biochemical findings of the cherry-red spot-myoclonus syndrome. She had 20/50 acuity in each eye, flutter-like ocular oscillations, rebound nystagmus, and transient vertical dissociation. Cherry-red maculas and optic atrophy were present. Although electroretinographic signals were normal, visual evoked potentials were almost absent. Levels of neuraminidase were significantly reduced in cultured ebroblasts from the patient and her parents, while lysosomal inclusions probably containing oligosaccharides were found in her conjunctival fibroblasts.

Adolescent↗
PubMed1978

Sequential interaction of macrophages, initiator T lymphocytes and recruited T lymphocytes in a cell-mediated immune response to soluble antigen.

We have investigated the sequential interaction of macrophages, initiator T lymphocytes (ITL) and recruited T lymphocytes (RTL) in the development of a T cell-mediated response to soluble antigens. Macrophages were pulsed with soluble antigens and used to sensitize ITL in vitro. The ITL were irradiated to prevent their proliferation and then injected into the footpads of syngeneic mice. Sensitized ITL were found to recruit immunospecific RTL in the draining lymph nodes, as determined by a thymidine uptake assay of the lymph node cells in vitro. The richest source of lymphocytes with ITL activity was the thymus, and progressively less activity was detectable among spleen or lymph node lymphocytes. The magnitude of the subsequent RTL response could be modified by genetic differences between the ITL and the antigen-pulsed macrophages that were used to sensitize them. Thus, ITL conveyed an immunogenic signal to RTL whose magnitude reflected the genotype of the macrophages, but whose specificity was directed by determinants of the soluble antigen.

Animals↗