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Biomedical subjects

F S Kantor

Publications and source records attributed to F S Kantor.

At least 37 records · Page 2Linked to original sources
PubMed1992

Long-term protection of mice from Lyme disease by vaccination with OspA.

Mice vaccinated with recombinant outer surface protein A (OspA) have been shown to be protected from infection with Borrelia burgdorferi, the agent of Lyme disease, when sacrificed 14 days after challenge with an intradermal inoculum of the spirochete. To determine whether infection was not merely delayed and that protection was long-lasting, we sacrificed vaccinated mice 60, 120, and 180 days after challenge; and to determine whether vaccinated mice retained their immune state over long periods, we challenged mice with B. burgdorferi 60, 90, 120, and 150 days after vaccination. The results of both groups of experiments show that the mice remained free from infection and disease and extend the usefulness of OspA as a vaccine candidate for Lyme borreliosis.

Animals↗
PubMed1991

Molecular mapping of Osp-A mediated immunity against Borrelia burgdorferi, the agent of Lyme disease.

It is paradoxical that although antibodies to the outer surface protein (Osp) A of Borrelia burgdorferi protect mice against infection and that immunization of uninfected mice with Osp-A is protective, antibodies to Osp-A induced early in natural infection of mice are not curative. A region recognized by a neutralizing mAb is also recognized by sera from chronically infected or immunized mice but is not bound by sera from mice infected for 15 days. Infection in mice, despite the presence of early Osp-A antibody, may therefore be explained in part by the lack of response to this epitope. Sera from infected humans recognizes this region, although in this case the immune response to Osp-A occurs only late in infection. Nonetheless, the fact that both human sera and sera from mice immunized with Osp-A bind a conformationally dependent epitope that localizes to the same region tentatively suggests that humans are able to respond to a protective epitope and that an Osp-A-based vaccine may elicit protective immunity in humans.

Animals↗
PubMed1991

Protection of mice from Lyme borreliosis by oral vaccination with Escherichia coli expressing OspA.

Mice immunized with recombinant outer surface protein A (OspA) in Freund's adjuvant or with intraperitoneal injections of live Escherichia coli expressing OspA have been shown to be protected from infection with Borrelia burgdorferi. To investigate the efficacy of oral vaccination, C3H/He mice were inoculated with 10(8) live E. coli expressing recombinant OspA by gavage and boosted in a similar manner on days 10, 20, 30, and 40. The animals developed serum IgG antibodies to OspA by immunoblot and were protected from infection when challenged with 10(4) B. burgdorferi intradermally 14 days after the last boost. Control mice did not develop antibodies to OspA and were not protected against challenge infection. These results suggest that an oral preparation of recombinant OspA could potentially be used for vaccination.

Animals↗
PubMed1990

Protection of mice against the Lyme disease agent by immunizing with recombinant OspA.

Lyme borreliosis is a tick-borne illness caused by Borrelia burgdorferi. The gene for outer surface protein A (OspA) from B. burgdorferi strain N40 was cloned into an expression vector and expressed in Escherichia coli. C3H/HeJ mice actively immunized with live transformed E. coli or purified recombinant OspA protein produced antibodies to OspA and were protected from challenge with several strains of B. burgdorferi. Recombinant OspA is a candidate for a vaccine for Lyme borreliosis.

Animals↗
PubMed1990

A sensitive rosetting assay for detection of acetylcholine receptor antibodies using BC3H-1 cells: positive results in 'antibody-negative' myasthenia gravis.

Antibodies to acetylcholine receptor (AChR) were measured in a group of patients with myasthenia gravis (MG), some of whom had previously been classified as 'antibody negative' using the standard anti-AChR radioimmunoassay (RIA). AChR antibodies were measured using the rosetting assay, a new detection method which utilizes protein A-coated red blood cells and live BC3H-1 cells, a murine cell line which expresses muscle nicotinic AChR. The results of the rosetting assay were compared with those obtained in the anti-AChR RIA. 76% of all myasthenic sera tested showed rosetting at titers higher than any of the control sera (from patients with non-myasthenic neurologic disease and normal individuals). Of the myasthenic patients previously classified as 'antibody negative' in the RIA using human AChR, 71% demonstrated positive rosetting. There was no correlation between the anti-AChR antibody titer obtained in the rosetting assay and that obtained in the RIA using either human or denervated rat AChR. The results suggest that the rosetting assay may measure a subpopulation of antibodies that differs from those detected in the RIA.

Animals↗
PubMed1989

An immunodominant site of acetylcholine receptor in experimental myasthenia mapped with T lymphocyte clones and synthetic peptides.

Myasthenia gravis (MG) is an autoimmune disease of man caused by antibodies directed against the acetylcholine receptor (AChR). In the experimental model of MG in mice, murine experimental autoimmune myasthenia gravis (EAMG), an anti-AChR immune response is induced by immunization with Torpedo AChR, and anti-AChR antibodies. AChR-sensitized T cells, and neuromuscular dysfunction result. The production of antibodies to AChR is thymus-dependent. In order to define the epitopes of the AChR identified by AChR-specific T cells, we generated T cell populations and T cell hybridoma clones and tested their reactivity to synthetic uniform-sized overlapping peptides representing the entire extracellular portion of the alpha-chain of the AChR. The predominant reactivity of the T cell clones and the parent lines was to a peptide corresponding to residues 146-162 of Torpedo AChR. This data is consistent with a highly limited recognition of AChR determinants in murine EAMG by AChR-specific T cells.

Animals↗
PubMed1985

Cellular cooperation in the expression of murine delayed-type hypersensitivity (DTH). 1. A normal accessory cell population enhances DTH produced by immune peritoneal exudate T lymphocytes.

A murine system for local passive transfer of delayed-type hypersensitivity (DTH) has recently been described. It was determined that untreated and T-lymphocyte-enriched (nylon-wool-nonadherent) fractions of peritoneal exudate (PE) cells from immunized donors could be transferred with soluble antigen to normal recipient footpads to efficiently produce a local DTH response. Untreated spleen or lymph node (LN) cell populations were strikingly less capable in this regard. It is now reported that addition of normal untreated PE cell populations to immune T-enriched PE cells markedly enhanced the DTH response transferred by the latter. Specific swelling was dose dependent with respect to each cell type. Removal of T lymphocytes from the normal PE cell population did not affect its enhancement of DTH. By cotransfer of 1 X 10(7) normal PE cells, significant specific swelling was obtained using 1-3 X 10(5) T-enriched immune PE cells. This represented a three- to seven-fold reduction in the requirement for the latter cell type. This scheme of DTH enhancement was employed to evaluate the mechanisms for decreased capability of immune LN and spleen for DTH transfer when compared to PE. No evidence was found that either adherent or nonadherent suppressor cells are operative at the time of DTH expression. Cotransfer of a DTH-enhancing population failed to equalize DTH expression by LN and spleen with that of PE. It is concluded that DTH effector-T-cell activity is enriched in immune peritoneal exudate and that non-T-cell population(s) from that source actively enhance DTH expression.

Animals↗
PubMed1985

Helper T-cell lines specific for the acetylcholine receptor: induction, characterization, and in vitro effects.

A strong immune response to the acetylcholine receptor (AChR), involving both cell-mediated and humoral immunity, underlies both myasthenia gravis and its experimental models. A central cell in this response and in its regulation is the helper-proliferative T-cell specific for the AChR. We have produced long-lived lines of these cells derived from mice immunized with AChR. These cells proliferate in an antigen-specific manner to the AChR, bear the Lyl and Thy markers, and lack the Ly23 antigen. Finally, these cells and their supernatants help primed B cells make anti-AChR antibody. These cells will provide us with a necessary tool for the dissection of mechanisms regulating the immune response to the AChR.

Animals↗
PubMed1984

In vitro and in vivo actions of acetylcholine receptor educated suppressor T cell lines in murine experimental autoimmune myasthenia gravis.

Immunization of C57Bl/6 mice with Torpedo acetylcholine receptor (AChR) leads to EAMG, experimental autoimmune myasthenia gravis, with characteristic clinical, electrophysiological, and immune features. Present in the lymphoid organs of mice with EAMG are AChR specific suppressor T cells: these cells can be grown in vitro as T cell lines. These lines are able to suppress the in vitro response to AChR, and can suppress the in vivo development of EAMG.

Animals↗
PubMed1983

The relation of clinical disease to antibody titre, proliferative response and neurophysiology in murine experimental autoimmune myasthenia gravis.

Murine myasthenia is a relatively faithful model of the human disease. We studied anti-AChR antibody titres, lymphocyte proliferative response to AChR, characteristic electromyographic (EMG) abnormalities and muscle strength at weekly intervals after immunization of C57B16J mice with Torpedo AChR. The boosting immunization at 1 month after the primary immunization resulted in a progressive increase of anti-AChR IgG antibodies, but caused a marked drop in the proliferative response. Although characteristic EMG abnormalities occurred in nearly all immunized mice, clinical disease appeared very late or not at all. These data parallel findings in human myasthenia.

Acetylcholine↗
PubMed1982

Nerve stimulation test in murine experimental autoimmune myasthenia gravis.

Use of the mouse model of myasthenia gravis (murine EAMG), ideally suited for immunological study, has been hampered by the relatively mild character of the disease and by the extended time and effort required for inducing severe disease. Electromyographic measurement of the compound action potential after repetitive stimuli, the nerve stimulation test, was evaluated for its ability to diagnose neuromuscular transmission defects in mice immunized with Torpedo acetylcholine receptor. With the combination of provocative maneuvers and raising of the body temperature, EAMG could be diagnosed in nearly all immunized animals a few weeks after immunization, whereas clinical evaluation of muscle weakness was positive in less than half of immunized mice months after the first immunization. Thus, EMG provides a means of objective evaluation of the disease and attempts at its experimental modification.

Animals↗
PubMed1982

Local passive transfer of delayed-type hypersensitivity in the mouse.

A means for local passive transfer of DTH in the mouse has been discovered and partially characterized. Briefly, peritoneal exudates (PE) are induced with incomplete Freund's adjuvant 5 to 7 days after immunization with antigen (usually picGPA) emulsified with complete Freund's adjuvant. Five days later, PE cells are harvested and transferred with soluble antigen into a hind footpad of a naive mouse. Antigen-specific swelling is defined as the change in diameter of footpads over the 24 hr after injection of PE cells plus immunizing antigen minus change in diameter of footpads injected with PE cells plus control antigen. Antigen-specific footpad swelling of 20 to 80% was found in contrast to meager swelling when lymph node or spleen cells were used. The magnitude was dependent on dose of both cells and antigen over a broad range (1 to 12 X 10(6) cells, 1 to 100 micrograms of antigen per recipient). Specific swelling was reduced to nil after treatment of PE cells with anti-theta serum, indicating T cell dependence. Carrier specificity of the response was similar to DTH in the guinea pig. Time course and histology are compatible with a DTH response as well. The superiority of PE cells in local transfer of DTH and the modest requirements of this murine local transfer system provide potent tools for identification of the cell(s) that mediate DTH and their interactions. This system, in addition, should provide a sensitive indicator of immunomodulating activity in cellfree supernatants.

Animals↗
PubMed1976

A canine distemper model of virus-induced anergy.

For development of an animal model of virus-induced anergy, the effect of canine distemper virus (CDV) upon cell-mediated immunity in dogs was investigated. First, canine cutaneous reactions and in vitro lymphocyte responses to soluble protein antigens were characterized. Dogs immunized with picryl guinea pig albumin and with keyhole limpet hemocyanin (both in complete Freund's adjuvant) responded reproducibly to intracutaneous challenge with these antigens. Reactivity peaked in 20-40 days (maximal induration, 6-50 mm). Lymphocytes from these animals responded in vitro to stimulation with keyhole limpet hemocyanin or purified protein derivative. This stimulation was antigen-specific and was maximal on day 6 of culture. Infection with CDV depressed cutaneous reactivity and lymphocyte response in vitro to antigens and mitogens. This effect was transient in animals previously vaccinated with attenuated CDV; however, gnotobiotic puppies (susceptible to CDV) had prolonged depression of cell-mediated immunity and lymphopenia. Some of these animals developed neurologic symptoms and died. The findings indicate that CDV infection is a potentially useful model for study of virus-induced depression of T (thymus)-cell responses and support the hypothesis that there is more than one mechanism responsible for this phenomenon.

Animals↗
PubMed1976

Sarcoid.

Patients with sarcoidosis were separated into those treated or not treated with prednisone. Skin test reactivity of both groups was clearly diminished but a significant decrease in T-cells was seen only in the steroid-treated group and this was not sufficient to explain the profound energy. Lymphocyte stimulation studies generally revealed elevated baseline incorporation of [3H]thymidine and reduced stimulation. Factors were present in the plasmsa of 1/4 to 1/3 of the patients which suppressed normal lymphocyte stimulation. When cells from 3 sarcoid patients were precultured in vitro, recovery towards normal occurred with a drop of the elevated baseline and rise in peak response.

Adult↗