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Biomedical subjects

D Teitelbaum

Publications and source records attributed to D Teitelbaum.

At least 55 records · Page 3Linked to original sources
PubMed1984

In vivo effects of antibodies against a high frequency idiotype of anti-DNA antibodies in MRL mice.

The in vivo effects of a rabbit antiserum against the dominant idiotype of MRL-lpr/lpr anti-DNA antibodies (termed H130) were studied in MRL-lpr/lpr, MRL/++, and BALB/c mice. Under the conditions we examined, the anti-idiotype did not suppress anti-DNA antibodies or the H130 idiotype in either MRL-lpr/lpr or MRL/++ mice. By contrast, MRL/++ and BALB/c mice responded to the antiserum by producing antibodies with the H130 idiotype. The increase in levels of the idiotype was accompanied by a rise in anti-DNA antibodies only when F(ab')2 fragments of the rabbit antiserum were administered. Only about 10% of the induced H130+ immunoglobulins were anti-DNA antibodies. An immunoregulatory disturbance in MRL-lpr/lpr mice may account for their resistance to anti-idiotypic antibodies. Treatment of autoimmune diseases with anti-idiotypes may have the undesired effect of augmenting the production of autoantibodies.

Animals↗
PubMed1983

Cell-mediated immunity to nervous system antigens in diabetic patients with neuropathy.

We investigated the presence of cell-mediated immunity to neural antigen in diabetes mellitus. The lymphocytes were tested for sensitization to purified antigens of the central and peripheral nervous systems by measuring specific transformation in vitro. The antigens used were a CNS basic encephalitogenic protein and P2, a peripheral nerve basic protein. Of the 40 insulin-requiring diabetes patients, 24 showed clinical manifestations of diabetic neuropathy, and the 16 patients without neuropathy served as a control group. Of the 24 neuropathic patients, 15 showed a positive lymphocyte stimulation index to either one or both antigens, whereas of the 16 control patients only one showed a positive index, and to the P2 antigen only. These findings suggest that cell-mediated autoimmunity may play a role in the pathogenesis of diabetic neuropathy.

Autoantibodies↗
PubMed1983

Immunomodulatory activities of human leukocyte interferon in advanced cancer patients.

Natural killing and antibody-dependent cellular cytotoxicity of peripheral blood lymphocytes from 33 advanced cancer patients were monitored during the course of treatment with human leukocyte interferon in a phase I trial. Ten patients receiving 10 to 60 X 10(6) international units (IU)/m2 in a single injection showed augmentation of cytolytic activity above pretreatment values. The most typical response consisted of a decrease in activity at day 1 followed by a significant increase on day 3 with a return to baseline at day 7. No clearcut minimal immunomodulatory dose was achieved, although four of six patients treated at 60 X 10(6) IU/m6 showed increased activity at day 3. Of these, three subsequently received repeated 60 X 10(6) IU/m2 doses on a weekly basis, and two of these showed repetitive augmentation after 3-4 weeks.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1982

Multiple sclerosis: trial of a synthetic polypeptide.

A synthetic polypeptide, copolymer I (COP I), composed of alanine, glutamic acid, lysine, and tyrosine, has been demonstrated to be nonencephalitogenic and nontoxic in laboratory animals, yet it is capable of suppressing experimental allergic encephalomyelitis. A preliminary open trial examined the ability of COP I to alter the course of disease in 12 patients with chronic progressive and 4 with exacerbating-remitting multiple sclerosis (MS). After therapy for as long as two years or more, no undesirable side reaction was noted in any patient. Three patients with chronic progressive MS and 2 with exacerbating-remitting disease are better. These results, which may represent simply a placebo effect or may be a significant response, are now being examined in randomized, placebo-controlled, double-blind pilot trials.

Adult↗
PubMed1982

Lack of H-2 restriction of suppressor factor specific to myelin basic encephalitogen.

A cell-free extract has been prepared from spleen cells of (SJL/J x BALB/c)F1 mice which were rendered non-susceptible to EAE by treatment with mouse spinal cord homogenate in incomplete Freund's adjuvant. Such extract has been previously shown to have suppressive activity on the induction of EAE, as well as on the immune response in syngeneic mice towards the mouse basic protein. We have now demonstrated that this factor is as effective in several other strains of mice, of different H-2 haplotype. The activity of this factor was manifested both in vivo by inhibiting the DTH response to MBE in the various mouse strains, and in vitro, by blocking the MIF activity of the allogeneic lymphocytes. A suppressor factor was prepared by a similar procedure from the EAE-resistant BALB/c mice. This factor was as active as the factor from the (SJL/J x BALB/c)F1 hybrid in blocking the anti-MBE antibody binding to MBE. It is also suppressive, and it inhibited the DTH response to MBE in both syngeneic and semi-allogeneic (SJL/J x BALB/c)F1 mice. It is thus demonstrated that the MBE-specific soluble suppressor factor involved in the EAE system in mice shows no indication of H-2 restriction.

Animals↗
PubMed1981

The immunologic response in mice unresponsive to experimental allergic encephalomyelitis.

The suppressor cells that are involved in antigen-induced protection against EAE in mice were investigated with respect to their effect on the immune response. The cellular immune response to the basic encephalitogenic protein (BE) and to PPD were studied in mice with either actively induced or adoptively transferred unresponsiveness to EAE. The results demonstrate that the DTH response to BE, as assayed in the radiometric ear skin test, was suppressed in mice protected against EAE. Moreover, the passive transfer of DTH response to BE by effector lymphocytes was also inhibited by the preinjection of suppressor cells. On the other hand, the suppressor cells did not affect the response to PPD in all these experiments. The results indicate that suppressor cells that mediate unresponsiveness to EAE regulate also the cellular immune response to BE in a specific manner. These suppressor cells are probably active both at the induction and the effector phase of the immune response.

Animals↗
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

The effect of Cop 1, a synthetic polypeptide, on chronic relapsing experimental allergic encephalomyelitis in guinea pigs.

Cop 1, a synthetic polypeptide, was evaluated for its effect on a chronic relapsing form of experimental allergic encephalomyelitis (EAE). Pretreatment of juvenile Strain 13 guinea pigs with Cop 1 in incomplete Freund's adjuvant (IFA) which were subsequently challenged with guinea pig spinal cord in complete Freund's adjuvant (CFA) had a marked effect in delaying or preventing the appearance of clinical signs of EAE. Administration of Cop 1 on appearance of clinical signs of EAE prevented progression of the first episode of the disease. Although relapses were not always prevented, they were modified on their duration and intensity both clinically and histologically.

Animals↗
PubMed1979

Effect of cyclophosphamide on suppressor cell activity in mice unresponsive to EAE.

Protection against experimental allergic encephalomyelitis (EAE) was induced in susceptible mice of (SJL/J X BALB/c)F1 hybrid, by injection of either mouse spinal cord homogenate, the small mouse basic protein, or Cop 1 in incomplete Freund's adjuvant, before EAE induction. It was demonstrated that the unresponsiveness induced by the three antigens is mediated by suppressor T cells residing in the spleen cell population and can be adoptively transferred to normal syngeneic recipients. Low dose of cyclophosphamide (20 mg/kg) administered 2 days before the encephalitogenic challenge abrogated the unresponsiveness to EAE and reverted the protected mice sensitive to disease induction. Cyclophosphamide was also active on adoptively transferred unresponsiveness, thus donors that had been treated with cyclophosphamide were unable to further transfer unresponsiveness to EAE. These results indicate the elimination by cyclophosphamide of suppressor cells that interfere with the effector mechanisms leading to EAE.

Animals↗