Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of different adjuvant formulations and routes of immunization on the antibody responses and protection induced in mice was determined by a synthetic peptide representing T- and B- cell epitopes from the measles virus (MV) fusion (F) protein (TTB peptide) which has previously been shown to induce protective responses against MV encephalitis in mice. When the peptide TTB was administered in Freud's complete adjuvant (FCA), Freud's incomplete adjuvant (FIA), alum or with IL-2, anti-peptide antibody responses and anti-MV antibody responses were detected. Interestingly, immunization with TTB without adjuvant resulted in the induction of anti-peptide antibody responses which did not cross react with the MV. The use of FIA as an adjuvant led to a significantly higher IgG2a antibody response compared with FCA and alum, whereas alum led to a significantly lower IgG3 response. Immunization with TTB in FCA, FIA and alum led to the generation of high affinity antibodies (with alum generating the highest affinity), whereas immunization of peptide with IL-2 or in PBS resulted in the induction of antibodies of lower affinity. Only the FCA, FIA and alum formulations led to the induction of protective responses in mice against MV-induced encephalitis. When the subcutaneous route (s.c.) of immunization was compared with the intraperitoneal route (i.p.), s.c. immunization with the TTB peptide led to higher anti-peptide and anti-MV antibody responses and higher affinity antibodies compared to those induced following i.p. immunization. Mice receiving the TTB peptide via the s.c. route had a higher percentage survival after MV challenge than those immunized via the i.p. route. These results show that the nature of the adjuvant used as well as the route of immunization play an important role in the induction of protective anti-TTB peptide antibody responses against MV-induced encephalitis in mice.
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PMID:Immunological analysis of the protective responses to the chimeric synthetic peptide representing T- and B-cell epitopes from the fusion protein of measles virus. 880 85

Mesothelioma usually leads to death within 8-14 months of diagnosis. To increase the potency of oncolytic measles viruses (MVs) for mesothelioma therapy, we inserted the interferon beta (IFNbeta) gene alone or with the human thyroidal sodium iodide symporter (NIS) gene into attenuated MV of the Edmonston lineage. The corresponding mouse IFNbeta (mIFNbeta) viruses, MV-mIFNbeta and MV-mIFNbeta-NIS, successfully propagated in human mesothelioma cells, leading to intercellular fusion and cell death. High levels of mIFNbeta were detected in the supernatants of the infected cells, and radioiodine uptake was substantial in the cells infected with MV-mIFNbeta-NIS. MV with mIFNbeta expression triggered CD68-positive immune cell infiltration 2-4 times higher than MV-GFP injected into the tumor site. The numbers of CD31-positive vascular endothelial cells within the tumor were decreased at day 7 after intratumoral injection of MV-mIFNbeta or MV-mIFNbeta-NIS, but not after MV-GFP and PBS administration. Immunohistochemical analysis showed that MV-mIFNbeta changed the microenvironment of the mesothelioma by increasing innate immune cell infiltration and inhibiting tumor angiogenesis. Oncolytic MVs coding for IFNbeta effectively retarded growth of human mesotheliomas and prolonged survival time in several mesothelioma tumor models. The results suggest that oncolytic MVs that code for IFNbeta and NIS will be potent and versatile agents for the treatment of human mesothelioma.
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PMID:Oncolytic measles viruses encoding interferon beta and the thyroidal sodium iodide symporter gene for mesothelioma virotherapy. 2037 24

Erysipelothrix rhusiopathiae (E. rhusiopathiae) is the causative agent of swine erysipelas. This microbe has caused great economic losses in China and in other countries. In this study, high-throughput cDNA microarray assays were employed to evaluate the host responses of porcine heart to E. rhusiopathiae and to gain additional insights into its pathogenesis. A total of 394 DE transcripts were detected in the active virulent E. rhusiopathiae infection group compared with the PBS group at 4 days post-infection. Moreover, 262 transcripts were upregulated and 132 transcripts were downregulated. Differentially expressed genes were involved in many vital functional classes, including inflammatory and immune responses, signal transduction, apoptosis, transport, protein phosphorylation and dephosphorylation, metabolic processes, chemotaxis, cell adhesion, and innate immune responses. Pathway analysis demonstrated that the most significant pathways were Chemokine signaling pathway, NF-kappa B signaling pathway, TLR pathway, CAMs, systemic lupus erythematosus, chemokine signaling pathway, Cytokine-cytokine receptor interaction, PI3K-Akt signaling pathway, Phagosome, HTLV-I infection, Measles, Rheumatoid arthritis and natural-killer-cell-mediated cytotoxicity. The reliability of our microarray data was verified by performing quantitative real-time PCR. This study is the first to document the response of piglet heart to E. rhusiopathiae infection. The observed gene expression profile could help screen potential host agents that can reduce the prevalence of E. rhusiopathiae. The profile might also provide insights into the underlying pathological changes that occur in pigs infected with E. rhusiopathiae.
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PMID:Transcription analysis of the responses of porcine heart to Erysipelothrix rhusiopathiae. 2897 97