The Experts below are selected from a list of 153 Experts worldwide ranked by ideXlab platform
Morten Frisch - One of the best experts on this subject based on the ideXlab platform.
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cytokines autoAntibodies and Viral Antibodies in premorbid and postdiagnostic sera from patients with rheumatoid arthritis case control study nested in a cohort of norwegian blood donors
Annals of the Rheumatic Diseases, 2008Co-Authors: Kristian Tore Jorgensen, Allan Wiik, Merete Pedersen, Chris Juul Hedegaard, Bent Faber Vestergaard, Randi Gislefoss, Tore K Kvien, Jan Wohlfahrt, Klaus Bendtzen, Morten FrischAbstract:Objective: To assess the timing of changes in cytokines, cytokine-related markers, autoAntibodies and Viral Antibodies in the pathogenesis of rheumatoid arthritis (RA). Methods: Case–control study nested in a prospective cohort of 31 330 blood donors in Oslo, Norway. Forty-nine donors developed RA up to 23 years after their most recent blood donation. Stored sera from these donors (case sera) and a sex- and age-matched sample of 245 healthy donors (control sera), and postdiagnostic sera from 33 of the 49 RA cases, were analysed for a panel of cytokines and cytokine-related markers, autoAntibodies and Antibodies against Epstein–Barr virus and parvovirus B19. Results: Cytokines and cytokine-related markers were generally negative in case sera from >5 years before the diagnosis of RA. In the 5-year interval immediately before the diagnosis of RA, more case than control sera were positive (odds ratios >2) for interleukin (IL)-1α, IL-1β, IL-1 receptor antagonist, IL-4, IL-10, tumour necrosis factor-α and soluble tumour necrosis factor receptor I. In postdiagnostic sera, however, 11 of 16 examined cytokines and cytokine-related markers were statistically significantly elevated compared with control sera. Seropositivity for IgG Antibodies against cyclic citrullinated peptides and for IgM and IgA rheumatoid factors were seen in case sera from up to 18 years before the diagnosis of RA. IgG Antibodies against Epstein–Barr virus and parvovirus B19 did not differ significantly between case and control sera. Conclusions: Cytokines and cytokine-related markers appear to be upregulated rather late in RA pathogenesis. In contrast, IgM rheumatoid factor and IgG anti-cyclic citrullinated peptide autoAntibodies may precede the diagnosis of RA by up to two decades.
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Cytokines, autoAntibodies and Viral Antibodies in premorbid and postdiagnostic sera from patients with rheumatoid arthritis: case–control study nested in a cohort of Norwegian blood donors
Annals of the Rheumatic Diseases, 2007Co-Authors: Kristian Tore Jorgensen, Allan Wiik, Merete Pedersen, Chris Juul Hedegaard, Bent Faber Vestergaard, Randi Gislefoss, Tore K Kvien, Jan Wohlfahrt, Klaus Bendtzen, Morten FrischAbstract:Objective: To assess the timing of changes in cytokines, cytokine-related markers, autoAntibodies and Viral Antibodies in the pathogenesis of rheumatoid arthritis (RA). Methods: Case–control study nested in a prospective cohort of 31 330 blood donors in Oslo, Norway. Forty-nine donors developed RA up to 23 years after their most recent blood donation. Stored sera from these donors (case sera) and a sex- and age-matched sample of 245 healthy donors (control sera), and postdiagnostic sera from 33 of the 49 RA cases, were analysed for a panel of cytokines and cytokine-related markers, autoAntibodies and Antibodies against Epstein–Barr virus and parvovirus B19. Results: Cytokines and cytokine-related markers were generally negative in case sera from >5 years before the diagnosis of RA. In the 5-year interval immediately before the diagnosis of RA, more case than control sera were positive (odds ratios >2) for interleukin (IL)-1α, IL-1β, IL-1 receptor antagonist, IL-4, IL-10, tumour necrosis factor-α and soluble tumour necrosis factor receptor I. In postdiagnostic sera, however, 11 of 16 examined cytokines and cytokine-related markers were statistically significantly elevated compared with control sera. Seropositivity for IgG Antibodies against cyclic citrullinated peptides and for IgM and IgA rheumatoid factors were seen in case sera from up to 18 years before the diagnosis of RA. IgG Antibodies against Epstein–Barr virus and parvovirus B19 did not differ significantly between case and control sera. Conclusions: Cytokines and cytokine-related markers appear to be upregulated rather late in RA pathogenesis. In contrast, IgM rheumatoid factor and IgG anti-cyclic citrullinated peptide autoAntibodies may precede the diagnosis of RA by up to two decades.
D. G. Harnish - One of the best experts on this subject based on the ideXlab platform.
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The nucleoprotein of Pichinde virus expressed by a vaccinia-Pichinde virus recombinant partially protects hamsters from lethal virus challenge
Archives of Virology, 1994Co-Authors: D. Y. Ozols, W. E. Rawls, K. L. Rosenthal, D. G. HarnishAbstract:Syrian hamsters, strain MHA/Lak, are susceptible to intraperitoneal infection with Pichinde virus and die from an overwhelming viremia. We have studied the ability of a vaccinia-Pichinde recombinant virus expressing amino acids 51-561 of the Viral nucleoprotein (VVNP_51-561) to protect from lethal Pichinde virus infection. Priming with VVNP_51-561 significantly delayed mortality and increased final survival outcome after challenge with 2×10^3 pfu of Pichinde virus. This protection was not complete compared to priming with Pichinde virus in the footpad, which was not lethal and provided 100% protection. At a higher challenge dose of Pichinde virus, 2×10^4 pfu, immunization with VVNP_51-561 delayed mortality but did not increase final survival. The partial protection correlated with an early but not late reduction in infectious virus in serum, kidney and liver, and infectious centers in the spleen. Thus the immune response generated by VVNP_51-561 could initially control the infection, effectively reducing the virus inoculum. As the infection proceeded, virus replication could not be limited resulting in death in some hamsters. The partial protection did not appear to be mediated by anti-Viral Antibodies since these were not detected in the serum of VVNP_56-561-immunized hamsters. This finding appears to support the hypothesis that in many arenavirus infections cellular immunity is central to Viral clearance and protection from reinfection.
Kristian Tore Jorgensen - One of the best experts on this subject based on the ideXlab platform.
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cytokines autoAntibodies and Viral Antibodies in premorbid and postdiagnostic sera from patients with rheumatoid arthritis case control study nested in a cohort of norwegian blood donors
Annals of the Rheumatic Diseases, 2008Co-Authors: Kristian Tore Jorgensen, Allan Wiik, Merete Pedersen, Chris Juul Hedegaard, Bent Faber Vestergaard, Randi Gislefoss, Tore K Kvien, Jan Wohlfahrt, Klaus Bendtzen, Morten FrischAbstract:Objective: To assess the timing of changes in cytokines, cytokine-related markers, autoAntibodies and Viral Antibodies in the pathogenesis of rheumatoid arthritis (RA). Methods: Case–control study nested in a prospective cohort of 31 330 blood donors in Oslo, Norway. Forty-nine donors developed RA up to 23 years after their most recent blood donation. Stored sera from these donors (case sera) and a sex- and age-matched sample of 245 healthy donors (control sera), and postdiagnostic sera from 33 of the 49 RA cases, were analysed for a panel of cytokines and cytokine-related markers, autoAntibodies and Antibodies against Epstein–Barr virus and parvovirus B19. Results: Cytokines and cytokine-related markers were generally negative in case sera from >5 years before the diagnosis of RA. In the 5-year interval immediately before the diagnosis of RA, more case than control sera were positive (odds ratios >2) for interleukin (IL)-1α, IL-1β, IL-1 receptor antagonist, IL-4, IL-10, tumour necrosis factor-α and soluble tumour necrosis factor receptor I. In postdiagnostic sera, however, 11 of 16 examined cytokines and cytokine-related markers were statistically significantly elevated compared with control sera. Seropositivity for IgG Antibodies against cyclic citrullinated peptides and for IgM and IgA rheumatoid factors were seen in case sera from up to 18 years before the diagnosis of RA. IgG Antibodies against Epstein–Barr virus and parvovirus B19 did not differ significantly between case and control sera. Conclusions: Cytokines and cytokine-related markers appear to be upregulated rather late in RA pathogenesis. In contrast, IgM rheumatoid factor and IgG anti-cyclic citrullinated peptide autoAntibodies may precede the diagnosis of RA by up to two decades.
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Cytokines, autoAntibodies and Viral Antibodies in premorbid and postdiagnostic sera from patients with rheumatoid arthritis: case–control study nested in a cohort of Norwegian blood donors
Annals of the Rheumatic Diseases, 2007Co-Authors: Kristian Tore Jorgensen, Allan Wiik, Merete Pedersen, Chris Juul Hedegaard, Bent Faber Vestergaard, Randi Gislefoss, Tore K Kvien, Jan Wohlfahrt, Klaus Bendtzen, Morten FrischAbstract:Objective: To assess the timing of changes in cytokines, cytokine-related markers, autoAntibodies and Viral Antibodies in the pathogenesis of rheumatoid arthritis (RA). Methods: Case–control study nested in a prospective cohort of 31 330 blood donors in Oslo, Norway. Forty-nine donors developed RA up to 23 years after their most recent blood donation. Stored sera from these donors (case sera) and a sex- and age-matched sample of 245 healthy donors (control sera), and postdiagnostic sera from 33 of the 49 RA cases, were analysed for a panel of cytokines and cytokine-related markers, autoAntibodies and Antibodies against Epstein–Barr virus and parvovirus B19. Results: Cytokines and cytokine-related markers were generally negative in case sera from >5 years before the diagnosis of RA. In the 5-year interval immediately before the diagnosis of RA, more case than control sera were positive (odds ratios >2) for interleukin (IL)-1α, IL-1β, IL-1 receptor antagonist, IL-4, IL-10, tumour necrosis factor-α and soluble tumour necrosis factor receptor I. In postdiagnostic sera, however, 11 of 16 examined cytokines and cytokine-related markers were statistically significantly elevated compared with control sera. Seropositivity for IgG Antibodies against cyclic citrullinated peptides and for IgM and IgA rheumatoid factors were seen in case sera from up to 18 years before the diagnosis of RA. IgG Antibodies against Epstein–Barr virus and parvovirus B19 did not differ significantly between case and control sera. Conclusions: Cytokines and cytokine-related markers appear to be upregulated rather late in RA pathogenesis. In contrast, IgM rheumatoid factor and IgG anti-cyclic citrullinated peptide autoAntibodies may precede the diagnosis of RA by up to two decades.
Joshua Labaer - One of the best experts on this subject based on the ideXlab platform.
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Novel systematic virus antibody survey in new-onset type 1 diabetes by protein arrays
Diabetes, 2014Co-Authors: Xiaofang Bian, Desmond Schatz, Clive H. Wasserfall, M A Atkinson, Garrick Wallstrom, J. Qiu, Jason Steel, A Throop, J. Park, Joshua LabaerAbstract:The link between Viral infections and type 1 diabetes (T1D) has relied on testing single virus. Herein, we utilized a customizable protein microarray platform, Nucleic Acid Programmable Protein Array (NAPPA), to identify serological Antibodies against entire Viral proteomes. Viral protein arrays comprising the complete proteomes from 7 viruses (294 ORFs) previously associated with T1D and 410 ORFs from other common viruses were constructed. The sero-reactivities of IgG, IgA and IgM were assessed for 42 new onset T1D patients and 42 age/sex similar healthy individuals (12.64 ± 4.94 vs. 12.83 ±4.97, 50%). Responses to specific Viral proteins were detected and validated by ELISA. Interestingly, Antibodies to EBV predominated in cases vs. controls (88% vs. 52%; OR 6.7, 95% CI 2.2-20.5; p=0.0008), whereas mumps virus (98% vs. 95%; OR 2.1, 95% CI 0.2-23.5; p > 0.1) and rubella virus (52% vs. 60%; OR 0.7, 95% CI 0.3-1.8; p > 0.1) did not show significant difference in frequency. The EBV effect was especially notable for BKRF4 (Fig. 1). We similarly observed responses against dominant antigens such as VP1 from coxsackievirus and VP4 and VP6 from rotavirus. We collected a comprehensive T1D-related Viral ORFeome and established a multiplexed/ high-throughput platform to survey Viral Antibodies. This innovative protein array tool could be used in future efforts to better characterize the association of Viral infection to T1D development. (Figure presented) .
D. Y. Ozols - One of the best experts on this subject based on the ideXlab platform.
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The nucleoprotein of Pichinde virus expressed by a vaccinia-Pichinde virus recombinant partially protects hamsters from lethal virus challenge
Archives of Virology, 1994Co-Authors: D. Y. Ozols, W. E. Rawls, K. L. Rosenthal, D. G. HarnishAbstract:Syrian hamsters, strain MHA/Lak, are susceptible to intraperitoneal infection with Pichinde virus and die from an overwhelming viremia. We have studied the ability of a vaccinia-Pichinde recombinant virus expressing amino acids 51-561 of the Viral nucleoprotein (VVNP_51-561) to protect from lethal Pichinde virus infection. Priming with VVNP_51-561 significantly delayed mortality and increased final survival outcome after challenge with 2×10^3 pfu of Pichinde virus. This protection was not complete compared to priming with Pichinde virus in the footpad, which was not lethal and provided 100% protection. At a higher challenge dose of Pichinde virus, 2×10^4 pfu, immunization with VVNP_51-561 delayed mortality but did not increase final survival. The partial protection correlated with an early but not late reduction in infectious virus in serum, kidney and liver, and infectious centers in the spleen. Thus the immune response generated by VVNP_51-561 could initially control the infection, effectively reducing the virus inoculum. As the infection proceeded, virus replication could not be limited resulting in death in some hamsters. The partial protection did not appear to be mediated by anti-Viral Antibodies since these were not detected in the serum of VVNP_56-561-immunized hamsters. This finding appears to support the hypothesis that in many arenavirus infections cellular immunity is central to Viral clearance and protection from reinfection.
