DABIL-2 recombinant fusion toxin effect on lymphocyte- and macrophage-producing cytokine subpopulation cells in experimentally induced demyelinating disease in mice.

Context: We have reported previously that DAB389IL-2 recombinant fusion toxin targets IL-2R bearing CD4 cells, and suppresses demyelinating disease in acute (A) - and chronic (C) - experimental autoimmune encephalomyelitis (EAE) animal models of multiple sclerosis.

Objectives: The present study was undertaken to investigate the effect of DAB389IL-2 treatment on various cytokine-secreting cell populations in A-EAE and C-EAE mice.

Materials And Methods: The effects of DAB389IL-2 at doses of 200-, 800-, or 1600 kU administered i.

DAB389IL-2 suppresses autoimmune inflammation in the CNS and inhibits T cell-mediated lysis of glial target cells.

In multiple sclerosis (MS) and its rodent model, experimental autoimmune encephalomyelitis (EAE), activated CD4(+) T cells with upregulated IL-2R mediate inflammation and demyelination in the central nervous system (CNS). DAB(389)IL-2, a chimeric fusion protein of IL-2 and diphtheria toxin, inhibits human and rodent IL-2 activated T cells that express the high affinity interleukin-2 receptor. In the present study, DAB(389)IL-2 was used to treat rats with EAE.

Effect of millimeter waves and cyclophosphamide on cytokine regulation.

We have reported previously that millimeter waves (MMWs) protect T-cell functions from the toxic side effects of cyclophosphamide (CPA), an anticancer drug. Since the effect of MMWs has been reported to be mediated by endogenous opioids, the present study was undertaken to investigate the role of endogenous opioids in protection of T-cell functions by MMWs. The effect of MMWs (42.

Suppression of murine experimental autoimmune encephalomyelitis by interleukin-2 receptor targeted fusion toxin, DAB(389)IL-2.

Previously we have shown that DAB(389)IL-2, a recombinant fusion toxin targeting IL-2R bearing cells, suppressed disease in the rat experimental autoimmune encephalomyelitis (EAE) model of acute multiple sclerosis (MS). Our present study demonstrates that DAB(389)IL-2 can also effectively suppress acute (A)-EAE, relapsing (R)-EAE and chronic (C)-EAE in mouse demyelinating models. DAB(389)IL-2 significantly suppressed mitogenic proliferation of spleen cells while mutant fusion proteins DA(glu53)B(389)IL-2 and DAB(389)IL-2(8-10) did not.

Effect of DAB(389)IL-2 immunotoxin on the course of experimental autoimmune encephalomyelitis in Lewis rats.

Activated T cells express the high affinity interleukin 2 receptor (IL-2R also CD25) that binds interleukin 2 (IL-2) and transduces signals important for the proliferation and survival of these cells. We investigated the effect of the genetically engineered immunotoxin DAB(389)IL-2 on experimental autoimmune encephalomyelitis (EAE), an autoimmune disease of the central nervous system (CNS) mediated by activated myelin-reactive T cells. EAE is the most commonly used animal model of the human disease multiple sclerosis (MS).

The fork head transcription factor FKTF-1b from Strongyloides stercoralis restores DAF-16 developmental function to mutant Caenorhabditis elegans.

The purpose of this study was to determine whether Strongyloides stercoralis FKTF-1, a transcription factor of the FOXO/FKH family and the likely output of insulin/IGF signal transduction in that parasite, has the same or similar developmental regulatory capabilities as DAF-16, its structural ortholog in Caenorhabditis elegans. To this end, both splice variants of the fktf-1 message were expressed under the control of the daf-16alpha promoter in C. elegans carrying loss of function mutations in both daf-2 (the insulin/IGF receptor kinase) and daf-16.

Skeletal muscle myosin is the autoantigen for experimental autoimmune myositis.

Experimental autoimmune myositis (EAM) is a rodent model for human inflammatory muscle disease (IMD). It can be induced by immunization of rodents with skeletal muscle homogenate and adjuvant. The specific myositogenic autoantigen has not been clearly identified although some evidence points to skeletal muscle myosin.

IL-12 reverses the suppressive effect of the CD40 ligand blockade on experimental autoimmune encephalomyelitis (EAE).

Blockade of the CD40 ligand (CD40L)-CD40 interaction suppresses experimental autoimmune encephalomyelitis (EAE). Since this interaction induces IL-12, an essential cytokine for EAE induction, we hypothesized that CD40L blockade may suppress EAE through IL-12 inhibition. Here we show that exogenous IL-12 abolishes the ability of anti-CD40L monoclonal antibodies to prevent EAE.

Pathogenesis of neuroimmunologic diseases. Experimental models.

Animal models of autoimmune diseases have greatly improved our current understanding of the pathogenesis of human autoimmunity and have provided the potential for therapies based on manipulation of the immune system. In our laboratory, we have investigated the immunopathogenesis of autoimmune diseases of the nervous system and muscle. We have developed immune-based approaches for the suppression of experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS), and experimental autoimmune neuritis (EAN), a model for the Guillain-Barré syndrome (GBS).

In vitro assays elucidate peculiar kinetics of clindamycin action against Toxoplasma gondii.

In order to characterize the delayed effect of clindamycin and macrolide antibiotics against Toxoplasma gondii tachyzoites (E. R. Pfefferkorn and S.

Scanning electron microscopy of Setaria cervi adult male worms.

Scanning electron microscopy studies of adult Setaria cervi male worms showed the presence of horn-like lateral appendages and characteristic striated bands on the ventral side of the tail. All other features were indistinguishable from other members of the genus Setaria.

Evaluation of Setaria cervi antigen in the diagnosis of human filariasis.

Bovine filariid worm (Setaria cervi) antigen was evaluated for the immunodiagnosis of human filariasis. Patients with manifestations of filarial infection; [1) microfilaremia cases, (2) chronic clinical cases, (3) tropical pulmonary eosinophilia (TPE) cases) were taken for the investigations along with (4) normal endemic and non-endemic human subjects. CIEP, IFAT and ELISA tests were employed for detection of serum antibodies.

Liver function and plasma protein metabolism in rodent model of filariasis.

Rodent model of filariasis was developed by infecting Wistar rats with Litomosoides carinii. Liver function tests, plasma protein concentrations, and synthesis rates of liver-formed proteins were estimated in these rats at 63 and 90 days post-infection. At 63 days post-infection, aspartate aminotransferase and alkaline phosphatase were significantly increased.

Experimental chemotherapy of Angiostrongylus cantonensis infection in mice with flubendazole, levamisole, and their combination.

The efficacy of the drugs flubendazole, levamisole, and their combination was studied against Angiostrongylus cantonensis infection in mice. The drugs were evaluated on day 15 post infection. The efficacy was assessed by using single-dose and 5-dose treatment schedules.

Efficacy of UV-irradiated larval vaccine of Ancylostoma ceylanicum (Looss, 1911) in golden hamsters (Mesocricetus auratus).

A vaccination trial in golden hamsters with UV-irradiated infective larvae of Ancylostoma ceylanicum was attempted. One oral vaccination of hamsters with 100 infective larvae irradiated by means of UV-tube (390 nm) at different time intervals induced the development of resistance. As the time exposure of irradiation was increased, there was a corresponding decrease in the subsequent worm establishment.

Immunological evidence of chemotherapeutic action of mebendazole against Ancylostoma ceylanicum (Looss, 1911) in hamsters (Mesocricetus auratus).

The immunological responses in hamsters during treatment with mebendazole against Ancylostoma ceylanicum are studied. Indirect haemagglutination (IHA) counterimmunoelectrophoresis (CIEP), passive cutaneous anaphylaxis (PCA), foot pad swelling for immediate (ITH) and delayed (DTH) types of hypersensitivities were employed for measuring the responses. Serum antibody which was 1:32 before treatment increased to the maximum of 1:512 (control 1:128) on the 10th day and it declined subsequently.

Ancylostoma ceylanicum (Looss, 1911) in golden hamsters (Mesocricetus auratus): pathogenicity and humoral immune response to a primary infection.

The response of hamsters to Ancylostoma ceylanicum was studied between days 13 and 200 after infection. The infected hamsters showed signs of anaemia, particularly between the 13th and 60th days. A significant loss in body-weight in the infected animals was also observed during this period.

Studies on suspected clinical and experimental angiostrongyliasis: serological responses.

Serum antibodies in suspected angiostrongyliasis patient were detected by ELISA. The antibody titre was 1:51,200 in the serum and 1:6,400 in CSF with preadult A. cantonensis antigen.

Pulmonary superoxide dismutase activity in the mouse infected with Ancylostoma caninum larvae.

Albino mice were infected per os with 1000 infective larvae of Ancylostoma caninum and pulmonary superoxide dismutase activity was studied after completion of lung migration. The total superoxide dismutase activity per mg of lung protein was elevated by 15% in infected mice. Of the two forms of superoxide dismutases studied, that containing Cu-Zn was elevated by 44%.

The distribution of Angiostrongylus cantonensis (Chen) in the central nervous system of laboratory rats.

The distribution of preadult Angiostrongylus cantonensis helminths in various regions of the central nervous system of rats, infected with varying doses of larvae, was studied. A dose of 10 000 larvae proved to be lethal; the rats showed paralytic symptoms and loss of vision prior to death. A very low dose of 15 larvae also proved to be infective to the central nervous system.

Necator americanus in infant rabbits: complete development, humoral antibody, leukocyte response and serum protein changes following infection.

Necator americanus, originally isolated from man, developed completely in infant rabbits (RSG-1). This infection was serially passed in infant rabbits up to the 6th generation without using any immunosuppressant. Two day old infant rabbits demonstrated a high degree of susceptibility to N.