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Julius M. Cruse - One of the best experts on this subject based on the ideXlab platform.
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Decreased Humoral Antibody episodes of acute renal allograft rejection in recipients expressing the HLA-DQβ1*0202 allele.
Experimental and molecular pathology, 2012Co-Authors: Venkat K.r. Mannam, Mark F. Santos, Robert E. Lewis, Julius M. CruseAbstract:The present investigation was designed to show the effect of human leukocyte antigen (HLA) class II molecular allelic specificities in the recipient on the induction of Humoral Antibody rejection, identified by C4d peritubular capillary staining, as well as specific Antibody identified by Luminex technology. Major histocompatibility complex (MHC) class II molecules are expressed on dendritic cells, macrophages, and B lymphocytes and they present antigenic peptides to CD4 positive T lymphocytes. Human renal peritubular and glomerular capillaries express class II MHC molecules upon activation. Expression of class II molecules on renal microvascular endothelial cells exposes them to possible interaction with specific circulating antibodies. We hypothesize that HLA-DQβ1*0202 expression in recipients decreases the likelihood of Antibody-mediated renal allograft rejection. We found that 80% (=25) of DQ2 positive haplotype recipients failed to induce Humoral Antibody renal allograft rejection and 20% (n=25) of DQ2 positive haplotype recipients induced Humoral Antibody renal allograft rejection (p=0.008). By contrast, 48% (n=46) of DQ2 negative haplotype recipients failed to induce a Humoral Antibody component of renal allograft rejection and 52% (n=46) of DQ2 negative haplotype recipients induced Humoral Antibody-mediated renal allograft rejection. Our results suggest that recipients who express the DQβ1*0202 allele are less likely to induce a Humoral Antibody component of acute renal allograft rejection than are those expressing DQ1, DQ3, or DQ4 alleles. DQβ1*0202 allele expression in recipients could possibly be protective against acute Humoral allograft rejection and might serve as a future criterion in recipient selection and in appropriate therapy for acute renal rejection episodes.
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DRβ1*1501, DQβ1*0602 donor allelic haplotype and Humoral Antibody episodes of acute renal allograft rejection.
Experimental and molecular pathology, 2010Co-Authors: Morgan Cowan, Venkat K.r. Mannam, Robert E. Lewis, Taryn Green, Joshua Goodin, Steven A. Bigler, Julius M. CruseAbstract:Abstract The present investigation was designed to show the effect of molecular HLA class II DR and DQ allelic differences between donor and recipient on Humoral Antibody rejection identified by C4d peritubular capillary staining. The hypothesis is that expression of the DRβ1*1501, DQβ1*0602 allele in the donor kidney increases the likelihood of Humoral Antibody rejection. We found that 67% (n = 18) of DR15 and/or DQ6 haplotype donor kidneys induced Humoral Antibody renal allograft rejection; 35% (n = 40) of DR15 and/or DQ6 haplotype donor kidneys failed to induce Humoral Antibody renal allograft rejection (p = 0.02). 42% (n = 31) of C4d+ recipients had donors with DR15; 17% (n = 42) of C4d recipients had donors with HLA-DR15 (p = 0.01).We compared donor haplotype alleles of 4 C4d+ with 6 C4d− recipients by high resolution molecular typing; 3 of 4 C4d+ recipients had a donor with the DRβ1*1501/DQβ1*0602 allele. This allele was absent in all C4d− donors. 35% of C4d+ recipients had 2 DR mismatches when compared to 36% of C4d− recipients. Our results, suggest that the DRβ1*1501, DQβ1*0602 allele in the donor kidney increases the risk of Humoral Antibody episodes of acute rejection, and signals the need for C4d staining of renal biopsies. Future analysis of additional donor and recipient haplotypes will establish whether or not this is a useful predictor of Humoral rejection episodes.
Aramis Augusto Pinto - One of the best experts on this subject based on the ideXlab platform.
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experimental infection of newcastle disease virus in pigeons columba livia Humoral Antibody response contact transmission and viral genome shedding
Veterinary Microbiology, 2008Co-Authors: Adriano De Oliveira Torres Carrasco, Meire Christina Seki, Tânia De Freitas Raso, Antonio Carlos Paulillo, Aramis Augusto PintoAbstract:The aim of this study was to evaluate the Humoral Antibody response, the genome viral excretion and the contact transmission of pathogenic chicken origin Newcastle disease virus (NDV) from experimentally infected pigeons (Columba livia) to in-contact pigeon. The Antibody response to infection was assessed by the hemagglutination inhibition (HI) test and the genome viral excretion was detected by RT-PCR. Viral strain induced high Antibody levels, both in inoculated and in sentinel birds. The pathogenic viral strain for chickens was unable to produce clinical signs of the disease in experimentally infected pigeons, although it induced the Humoral Antibody response and produced NDV genome shedding. NDV genome was detected intermittently throughout the experimental period, from 5 days post-infection (dpi) to 24 dpi. Therefore, viral genome shedding occurred for 20 days. The viral genome was detected in all birds, between 11 and 13 dpi. Furthermore, the high infectivity of the virus was confirmed, as all non-inoculated sentinel pigeons showed Antibody levels as high as those of inoculated birds.
Bong-kyun Park - One of the best experts on this subject based on the ideXlab platform.
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Increased Humoral Antibody response of foot-and-mouth disease virus vaccine in growing pigs pre-treated with poly-γ-glutamic acid
Journal of veterinary science, 2016Co-Authors: Jeehoon Lee, Ikjae Kang, A-reum Kim, You-sun Noh, Hee-chun Chung, Bong-kyun ParkAbstract:This study was conducted to determine if Humoral Antibody response of foot-and-mouth disease (FMD) vaccine improved in 8-week-old growing pigs born to well-vaccinated sows pre-treated with 60 mg of poly-γ-glutamic acid (γ-PGA) three days before vaccination. Antibody against FMD virus serotype O was measured 0, 2, 4 and 6 weeks post-vaccination, using a PrioCHECK FMDV type O ELISA kit. The results showed that positive Antibody reactions against FMDV serotype O antigen among a component of the vaccine significantly increased in response to pre-injection with γ-PGA.
Julio Coll - One of the best experts on this subject based on the ideXlab platform.
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DNA vaccination by immersion and ultrasound to trout viral haemorrhagic septicaemia virus.
Vaccine, 2001Co-Authors: M. Fernandez-alonso, A.i. Rocha, Julio CollAbstract:This work reports preliminary data on the application of a novel method, ultrasound, for the DNA vaccination of rainbow trout. First, the best formulations were selected that increased the transfer by immersion of a plasmid coding for the green fluorescent protein (GFP) gene into trout fry. Quantification of GFP expression by fluorescence in the fin cells was used to study time course, DNA concentration dependence and comparison of different formulations. The best GFP expression results were obtained with short pulses of ultrasound, DOTAP liposomes and recombinant bacteria or bactofection. Other liposomes or microencapsulation formulations resulted in a GFP fluorescence similar to background values. Second, DNA immersion-vaccination of immunocompetent fingerling trout with the selected formulations was performed by using a plasmid coding for the glycoprotein G gene of the viral haemorrhagic septicaemia virus (VHSV). The immunization of fingerling trout was estimated by measuring Humoral Antibody, lymphoproliferation and VHSV challenge responses. Short pulses of low intensity ultrasound were the only method by which both Humoral Antibody responses and survival after VHSV challenge were obtained. Immersion DNA-vaccination using short pulses of ultrasound could eventually lead to a practical way to vaccinate small fish.
Amrita Dosanjh - One of the best experts on this subject based on the ideXlab platform.
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Chronic pediatric pulmonary disease and primary Humoral Antibody based immune disease.
Respiratory medicine, 2010Co-Authors: Amrita DosanjhAbstract:Summary Chronic inflammation of the larger airways is a common occurrence in children. A number of factors such as younger age, premature birth, male gender, exposure to environmental smoke or pollution, and crowded housing can increase a child's susceptibility to chronic lung disease. Chronic bronchitis may be caused by an underlying Humoral immunodeficiency if the clinical course is recurrent or prolonged. Primary Humoral immunodeficiency accounts for approximately 70% of all immunodeficiencies. The differential of chronic bronchitis also includes Cystic Fibrosis, ciliary defects and immune cellular and phagocytic defects. 1,2 This review will summarize the most common Humoral Antibody based immune based deficiencies associated with chronic pulmonary disease.
