DreamPharm Products:
Mol Ther. 2002 Sep;6(3):359-68.
Immune response to full-length dystrophin delivered to Dmd muscle by a high-capacity adenoviral vector.
Gilchrist SC, Ontell MP, Kochanek S, Clemens PR.
Department of Neurology, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA.
Adenoviral vector-mediated gene transfer to skeletal muscle is a promising potential treatment for Duchenne muscular dystrophy. However, the immunological response to viral antigens and the therapeutic protein expressed by the delivered gene could prevent effective treatment. In this study, we investigated the immune response induced by adenoviral and dystrophin antigens presented by high-capacity adenoviral vector-mediated dystrophin and beta-galactosidase delivery to skeletal muscle of a mouse model that is both dystrophin-deficient and lacZ transgenic. Direct intramuscular gene delivery of the high-capacity adenoviral vector encoding full-length murine dystrophin resulted in stable expression of recombinant dystrophin for 5 months in mice treated as neonates and for 4 weeks in mice treated as adults. We observed neutralizing antibody to adenoviral antigens only in mice treated as adults and not in mice treated as neonates. This suggested that adenoviral antigens were only presented at the time of vector administration when the neonatal immune system was not yet mature. In contrast, antibodies to dystrophin were observed both in mice treated as neonates and in mice treated as adults. The development of an anti-dystrophin antibody response in mice treated with the high-capacity adenoviral vector as neonates suggested that dystrophin antigens were presented to the immune system at a time remote from the gene delivery, when the immune system was mature. Interestingly, an antibody response against beta-galactosidase developed late in the course of mice treated with the high-capacity adenoviral vector as neonates, suggesting a loss of tolerance to beta-galactosidase, a self-antigen in these transgenic mice. Our results suggest that future human trials of dystrophin gene delivery will need to address the potential for immunity induced by ongoing segmental degeneration of partially treated muscle fibers and presentation of recombinant dystrophin antigens in the context of a Duchenne muscular dystrophy patient.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12231172&dopt=Abstract
Vaccine. 2003 Jan 30;21(7-8):798-801.
Towards new immunotherapies: targeting recombinant cytokines to the immune system using live attenuated Salmonella.
Rosenkranz CD, Chiara D, Agorio C, Baz A, Pasetti MF, Schreiber F, Dematteis S, Martinez M, Sztein MB, Chabalgoity JA.
Laboratory for Vaccine Research, Department of Biotechnology, Instituto de Higiene, Facultad de Medicina, Avda. A. Navarro 3051, CP 11200, Montevideo, Uruguay
We have used Salmonella as a delivery system for eukaryotic expression plasmids encoding cytokines, and assessed its capacity to modulate immune responses in different experimental models. Plasmids encoding mouse IL-4 and IL-18 under cytomegalovirus promoter were constructed and transformed into live attenuated Salmonella enterica serovar Typhi strain CVD 908-htrA, and Salmonella enterica serovar Typhimurium strain SL3261. We have shown that systemic as well as mucosal immunization with such constructs can influence the antibody and cytokine responses to the Salmonella carrier and to co-administered bystander antigens, as well as the specific immune response elicited during a parasitic infection. Further, we have shown that oral cytokine-therapy using Salmonella as gene vector induce antitumoral effect as demonstrated by extended survival time in melanoma-bearing mice.This approach may be particularly suited for the development of new immunotherapies with applications in parasitic infections and cancer, were alterations of the host's immune responses are usually found, and therapy-induced modulation of the immune response is likely to be required.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12531363&dopt=Abstract [PubMed - in process]
Cell Immunol. 2002 Jul-Aug;218(1-2):46-58.
Candida albicans infection enhances immunosuppression induced by cyclophosphamide by selective priming of suppressive myeloid progenitors for NO production.
Angulo I, Jimenez-Diaz MB, Garcia-Bustos JF, Gargallo D, de las Heras FG, Munoz-Fernandez MA, Fresno M.
Centro de Biologia Molecular, Severo Ochoa, CSIC-Universidad Autonoma de Madrid, Cantoblanco, 28049 Madrid, Spain.
Systemic infections caused by fungi after cytoreductive therapies are especially difficult to deal with in spite of currently available antimicrobials. However, little is known about the effects of fungi on the immune system of immunosuppressed hosts. We have addressed this by studying the in vitro T cell responses after systemic infection with Candida albicans in cyclophosphamide-treated mice. After cyclophosphamide treatment, a massive splenic colonization of the spleens, but not lymph nodes, by immature myeloid progenitor (Ly-6G(+)CD11b(+))cells is observed. These cells are able to suppress proliferation of T lymphocytes via a nitric oxide (NO)-dependent mechanism. Systemic infection with a sublethal dose of C. albicans did not cause immunosuppression per se but strongly increased NO-dependent suppression in cyclophosphamide-treated mice, by selective priming of suppressive myeloid progenitors (Ly-6G(+)CD11b(+)CD31(+)CD40(+)WGA(+)CD117(low/-)CD34(low/-)) for iNOS protein expression. The results indicate that systemic C. albicans infection can augment the effects of immunosuppressive therapies by promoting functional changes in immunosuppressive cells.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12470613&dopt=Abstract
J Nutr Biochem. 2002 Sep;13(9):539.
Total salivary IgA, serum C3c and IgA in obese school children.
Pallaro A, Barbeito S, Taberner P, Marino P, Franchello A, Strasnoy I, Ramos O, Slobodianik N.
Department Nutrition, School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina
Studies of the immunologic function in adult obese humans and experimental models indicate that excess adiposity is associated with impairments in host defense mechanisms. The aim of this work was to analyze the secretory and humoral immune system in obese children (n = 105, 55 boys, 50 girls ), between 6 and 13 years of age. Samples of non-stimulated saliva and whole blood were collected from fasting patients. Total salivary IgA (IgAsal), serum C3 complement (C3c) and Immunoglobulin A (IgA) were determined by quantitative radial immunodifussion on agar gel layers ( Diffu-plate, Biocienti;fica SA ). Results, expressed as mg/dl, were compared to laboratory reference values from healthy children of either sex in the same range of age that belong to the same socioeconomic class (n = 60). Data (Mean +/- 1 SD) of the whole population were: IgAsal: 11.4 +/- 4.8 vs 14.8 +/- 6.9; C3c: 190.7 +/- 53.1 vs 126.3 +/- 45.5; IgA: 194.5 +/- 101.5 vs 157.2 +/- 19.9. Data distribution showed higher frecuencies near the zone of the highest reference values for serum C3c; when results of IgA and IgAsal were expressed as percentage of the mean reference value, 51% and 48.6% of the whole studied population presented data lower than 100% and 75% respectively. These results show a compromised secretory immune system without incidence of clinical symptoms and infections, whereas humoral immunity might not be profoundly affected.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12231424&dopt=Abstract [PubMed - as supplied by publisher]
Kinetoplastid Biol Dis. 2002 May 20;1(1):1.
Molecular determinants and regulation of Leishmania virulence.
Chang KP, McGwire BS.
Department of Microbiology/Immunology, University of Health Sciences/Chicago Medical School, North Chicago, IL, USA. changinchcms.edu
A Leishmania model to explain microbial virulence in chronic infectious diseases is proposed. All these diseases progress from infection to symptomatic phase to host death or recovery. The outcome of each phase is depicted to result from the interactions of a distinct group of parasite molecules with a specific host immune compartment. The first group consists of invasive/evasive determinants, which are largely parasite cell surface and secreted molecules. Their activities help parasites establish infection by overcoming host immunologic and non-immunologic barriers. These determinants do not cause disease per se, but are indispensable for infection necessary for the development of a disease-state. The second group of parasite molecules consists of "pathoantigenic" determinants - unique parasite epitopes present often within otherwise highly conserved cytoplasmic molecules. Immune response against these determinants is thought to result in immunopathology manifested as clinical signs or symptoms, namely the virulent phenotype. The third group of parasite molecules is hypothetically perceived as vaccine determinants. Their interactions with the host immune system lead to the elimination or reduction of parasites to effect a clinical cure. Differential expression of these determinants alone by parasites may alter their interactions with the hosts. Virulent phenotype is consequently presented as a spectrum of manifestations from asymptomatic infection to fatality. A secondary level of regulation lies in host genetic and environmental factors. The model suggests that different parasite determinants may be targeted by different strategies to achieve more effective control of leishmaniasis and other similar diseases.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12234388&dopt=Abstract [PubMed - as supplied by publisher]
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