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Passive Transfer (passive + transfer)
Selected AbstractsBacterial Cell Penetration by ,3 -Oligohomoarginines: Indications for Passive Transfer through the Lipid BilayerCHEMBIOCHEM, Issue 6 2005Birgit Geueke Dr. Uptake of fluorescently labeled ,-oligohomoarginines amides by bacteria was examined with confocal laser scanning microscopy and fluorescence quenching assays. The results indicate that microorganisms, which have no endocytotic mechanisms for transmembrane transport, internalize the peptides through an unidentified alternative pathway (see micrograph). [source] What's new in bullous pemphigoidTHE JOURNAL OF DERMATOLOGY, Issue 3 2010Hideyuki UJIIE Abstract Bullous pemphigoid (BP) is the most common autoimmune blistering disease. BP patients have autoantibodies against type XVII collagen (COL17, also called BP180 or BPAG2), a type II transmembrane protein that spans the lamina lucida and projects into the lamina densa of the epidermal basement membrane. The non-collagenous 16A domain of COL17 is considered to contain pathogenic epitopes of BP. The transfer of immunoglobulin (Ig)G from BP patients fails to cause blisters on mouse skin probably due to differences between humans and mice in the amino acid sequence of NC16A pathogenic epitope of COL17. Passive transfer of rabbit IgG antibodies against the murine homolog of human COL17 NC16A triggers immune reactions to COL17 in mice, including complement activation, mast cell degranulation and neutrophilic infiltration, resulting in dermal,epidermal separation. Recent studies using COL17-humanized mice that express human COL17 but lack murine COL17 were the first to demonstrate the pathogenicity of anti-COL17 human BP IgG autoantibodies in vivo. These new findings provide a greater understanding of BP pathomechanisms and facilitate the development of novel specific and efficient therapeutic strategies for BP. [source] Mouse × pig chimeric antibodies expressed in Baculovirus retain the same properties of their parent antibodiesBIOTECHNOLOGY PROGRESS, Issue 2 2009Ana M. Jar Abstract The development of hybridoma and recombinant DNA technologies has made it possible to use antibodies against cancer, autoimmune disorders, and infectious diseases in humans. These advances in therapy, as well as immunoprophylaxis, could also make it possible to use these technologies in agricultural species of economic importance such as pigs. Porcine reproductive and respiratory syndrome virus (PRRSV) is an arterivirus causing very important economic losses to the industry. Passive transfer of antibodies obtained by biotechnology could be used in the future to complement or replace vaccination against this and other pig pathogens. To this end, we constructed and studied the properties of chimeric mouse × pig anti-PRRSV antibodies. We cloned the constant regions of gamma-1 and gamma-2 heavy chains and the lambda light chain of pig antibodies in frame with the variable regions of heavy and light chains of mouse monoclonal antibody ISU25C1, which has neutralizing activity against PRRSV. The coding regions for chimeric IgG1 and IgG2 were expressed in a baculovirus expression system. Both chimeric antibodies recognized PRRSV in ELISA as well as in a Western-blot format and, more importantly, were able to neutralize PRRSV in the same fashion as the parent mouse monoclonal antibody ISU25C1. In addition, we show that both pig IgG1 and IgG2 antibodies could bind complement component C1q, with IgG2 being more efficient than IgG1 in binding C1q. Expressing chimeric pig antibodies with protective capabilities offers a new alternative strategy for infectious disease control in domestic pigs. © 2009 American Institute of Chemical Engineers Biotechnol. Prog., 2009 [source] Exacerbation of experimental autoimmune encephalomyelitis in rodents infected with murine gammaherpesvirus-68EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 7 2003James Abstract Viral infections have long been suspected to play a role in the pathogenesis of multiple sclerosis. In the present study, two different rodent models of experimental autoimmune encephalomyelitis (EAE) were used to demonstrate the ability of murine gammaherpesvirus-68 (,HV-68) to exacerbate development of neurological symptoms. SJL mice received UV-inactivated ,HV-68 or intranasal,HV-68, followed by immunization against proteolipid-protein peptide 139,151. Infected mice became moribund within 10,days post-immunization, whereas mice exposed to UV-inactivated ,HV-68 recovered. In the second model, Lewis rats were exposed to UV-inactivated ,HV-68 or to ,HV-68, followed by passive transfer of encephalitogenic T lymphocytes specific for myelin basic protein. Consistently, infected rats had higher clinical scores, and this result was observed during acute or latent ,HV-68 infection. It is unlikely that this ,HV-68-induced exacerbation was due to significant viral replication within the central nervous system since nested PCR, viral plaque assays, and infectious-centers assays demonstrated no detectable virus in spinal cords or brains of infected rodents undergoing EAE. Taken together, these studies demonstrate increased clinical symptoms of EAE in rodents infected by a gammaherpesvirus that has a limited ability to invade the central nervous system. [source] Hepatitis C infection in children: A Melbourne perspectiveJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 4 2000B Karim Objective: To examine the clinical spectrum of hepatitis C virus (HCV) infected children in our care by determining presentation, mode of acquisition, degree of co-infection, biochemical evidence of persisting hepatitis and treatment outcome. Methodology: A retrospective review of the medical records of all children attending the Royal Children's Hospital, Melbourne, between 1990 and 1998, who had antibodies to HCV infection detected. Detailed clinical information, investigations and the results of treatment were extracted from the clinical notes. Results: A total of 94 children (age range 2 weeks to 19.7 years) were identified, of whom nine had passive transfer of maternal antibodies from HCV-positive mothers and were excluded from analysis. Sixty-seven children (79%) were infected by transfusion of blood or blood products. Perinatal transmission occurred in 11 children (13%), and six children (7%) had a history of i.v. drug abuse. The majority of children were asymptomatic at presentation. Of the 65 patients tested for HCV-ribonucleic acid, 43 (66%) were positive. Fifty-seven cases had serial alanine aminotransaminase (ALT) measurements over a mean of 28 months. Of these, 38 (67%) had an abnormal ALT. Ten cases (12%) were co-infected with hepatitis B virus, HIV or both. Of 12 patients treated with interferon, four responded with normalisation of ALT from 3 to 12 months post-commencement of therapy. Conclusions: Although HCV was largely an asymptomatic condition in our clinic population, more than half the patients had biochemical evidence of ongoing liver damage. Given the chronicity of this infection in the majority of patients and the long-term risks of cirrhosis and hepatocellular carcinoma, children with HCV infection represent a high-risk group worthy of regular follow up. [source] Serum IgG Concentrations after Intravenous Serum Transfusion in a Randomized Clinical Trial in Dairy Calves with Inadequate Transfer of Colostral ImmunoglobulinsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010M. Chigerwe Background: Plasma transfusions have been used clinically in the management of neonates with failure of passive transfer. No studies have evaluated the effect of IV serum transfusions on serum IgG concentrations in dairy calves with inadequate transfer of passive immunity. Hypothesis: A commercially available serum product will increase serum immunoglobulin concentration in calves with inadequate transfer of colostral immunoglobulins. Animals: Thirty-two Jersey and Jersey-Holstein cross calves with inadequate colostral transfer of immunoglobulins (serum total protein <5.0 g/L). Methods: Thirty-two calves were randomly assigned to either control (n = 15) or treated (n = 17) groups. Treated calves received 0.5 L of a pooled serum product IV. Serum IgG concentrations before and after serum transfusion were determined by radial immunodiffusion. Results: Serum protein concentrations increased from time 0 to 72 hours in both control and transfused calves and the difference was significant between the control and treatment groups (P < .001). Mean pre- and posttreatment serum IgG concentrations in control and transfused calves did not differ significantly. Median serum IgG concentrations decreased from 0 to 72 hours by 70 mg/dL in control calves and increased over the same time interval in transfused calves by 210 mg/dL. The difference was significant between groups (P < .001). The percentage of calves that had failure of immunoglobulin transfer 72 hours after serum transfusion was 82.4%. Conclusions and Clinical Importance: Serum administration at the dosage reported did not provide adequate serum IgG concentrations in neonatal calves with inadequate transfer of colostral immunoglobulins. [source] Serum Immunoglobulin G Concentrations in Calves Fed Fresh Colostrum or a Colostrum SupplementJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2002Nicole M. Holloway This study compared serum immunoglobulin G (IgG) concentrations in calves fed colostrum with those of calves fed a colostrum supplement containing spray-dried serum. Twenty-four Holstein calves were randomly assigned to 1 of 2 treatment groups (fresh colostrum or colostrum supplement). Each calf was fed 4 L of colostrum (n1= 12) or 4 L of colostrum supplement (n2= 12) via oroesophageal intubation at 3 hours of age. The concentration of the colostrum supplement fed to calves was twice the manufacturer's recommendation. The median and range values for colostral IgG concentration were 6,430 mg/dL and 1,400-17,000 mg/ dL, respectively. Median serum IgG concentrations at 2 days of age differed significantly (P= .001) between calves receiving fresh colostrum (3,350 mg/dL) and the colostrum supplement (643 mg/dL). Eight percent of calves force fed colostrum had serum IgG concentrations <1,000 mg/dL, whereas 75% of calves force-fed supplement had IgG concentrations below this threshold. The calculated population relative risks for mortality associated with passive transfer for calves force-fed colostrum and calves force-fed colostrum supplement were 1.09 and 1.90, respectively. Force-fed fresh colostrum is superior to the colostrum supplement studied, but the colostrum supplement has similar efficacy to routine colostrum administration practices. [source] CD40-expressing plasmid induces anti-CD40 antibody and enhances immune responses to DNA vaccinationTHE JOURNAL OF GENE MEDICINE, Issue 1 2010Hanqian Xu Abstract Background Various approaches have been used to improve the efficacy of DNA vaccination, including the incorporation of molecular adjuvants. Because the CD40 ligand,CD40 interaction plays a major role in initiating immune responses, we sought to develop a molecular adjuvant targeting this interaction. Methods and Results We immunized mice with a foot-and-mouth disease virus DNA vaccine, pcD-VP1, together with a CD40-expressing plasmid, pcD-CD40. We found that pcD-CD40 induced anti-CD40 antibodies, which temporally correlated with the augmented production of anti-VP1 antibody. pcD-CD40 similarly augmented the humoral response of another DNA vaccine that targets hepatitis B virus, and passive transfer of anti-CD40 antisera also showed a similar effect. Furthermore, the pcD-CD40-elicited anti-CD40 antibodies were able to activate the CD40 signal pathway in antigen-presenting cells in vitro, which led to the maturation of dendritic cells (DCs) and DC-mediated T cell activation. Thus, pcD-CD40 augments DNA vaccination by inducing anti-CD40 antibodies, which in turn promotes T cell activation. Conclusions This is the first reported ,proadjuvant' that augments DNA vaccination indirectly by eliciting agonistic antibodies. Copyright © 2009 John Wiley & Sons, Ltd. [source] Complement Independent Antibody-Mediated Endarteritis and Transplant Arteriopathy in MiceAMERICAN JOURNAL OF TRANSPLANTATION, Issue 3 2010T. Hirohashi Complement fixation, as evidenced by C4d in the microvasculature, is a widely accepted criterion of antibody-mediated rejection. Complement fixation has been shown to be essential in acute antibody-mediated rejection, but its role in chronic rejection has not been addressed. Previous studies showed that passive transfer of complement fixing monoclonal IgG2a anti-H-2Kk into B6.RAG1,/, KO recipients of B10.BR hearts led to progressive chronic transplant arteriopathy (CTA) over 14,28 days, accompanied by C4d deposition. The present studies were designed to test whether complement was required for these lesions. We report that a noncomplement fixing donor-specific alloantibody (DSA, monoclonal IgG1 anti-H-2Kk) injected into B6.RAG1 -/- KO recipients of B10.BR hearts also promotes CTA, without C4d deposition. Furthermore, a passive transfer of DSA (monoclonal IgG2a anti-H-2Kk) initiated endarteritis followed by CTA in B6.RAG1,/- mice genetically deficient in the third component of complement (RAG1,/,C3,/,). These studies indicate that antibody to class I MHC antigens can trigger chronic arterial lesions in vivo without complement participation, in contrast to acute antibody-mediated rejection. This pathway may be relevant to C4d-negative chronic rejection sometimes observed in patients with DSA, and argues that lack of C4d deposition does not exclude antibody-mediated chronic rejection. [source] Novel function of DUSP14/MKP6 (dual specific phosphatase 14) as a nonspecific regulatory molecule for delayed-type hypersensitivityBRITISH JOURNAL OF DERMATOLOGY, Issue 5 2007Y. Nakano Summary Background, Nonspecific unresponsive states of delayed-type hypersensitivity (DTH) to unrelated antigens are induced in mice by a single administration of hapten. In these studies, we found a unique regulatory mechanism of contact hypersensitivity (CHS) mediated by nonspecific suppressor factor (NSF) induced by the intravenous injection of hapten-conjugated syngeneic spleen cells. NSF is a , 45-kDa protein released from the macrophage-like suppressor cells and binds selectively to dendritic cells (DCs). Moreover, NSF-treated DCs release a second , 20-kDa NSF (NSFint). Objectives, To try and identify NSF and characterize its function. Methods, The suppressor activity was evaluated by inhibition of the passive transfer of CHS by the effector cells sensitized with hapten and the antigen-presenting cell (APC) activity of hapten-primed draining lymph node cells (DLNCs) to induce CHS. NSF-containing supernatants obtained from the culture of spleen cells from mice that had been injected intravenously with oxazolone-conjugated syngeneic spleen cells 7 days before were prepared and purified with a Green A dye-affinity column, DEAE column and Sephacryl S-200 column. Then, samples of molecular mass of , 45 kDa were separated by native-PAGE (polyacrylamide gel electrophoresis) and nonreducing sodium dodecyl sulphate (SDS)-PAGE. After confirming the suppressor activity of proteins of , 45 kDa separated by native-PAGE, samples were separated by nonreducing SDS-PAGE, transferred onto polyvinylidene difluoride membranes and analysed using matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry. Results, Proteins of , 45 kDa eluted from a Sephacryl S-200 column and the slice of native-PAGE gel exhibited the strong suppressor activity. Analyses using MALDI-TOF mass spectrometry and MASCOT algorithm of the protein bands around 45 kDa separated by nonreducing SDS-PAGE identified NSF as a 22·5-kDa protein, dual specific phosphatase 14/MAP-kinase phophatase-6 (DUSP14/MKP6), which functions as a negative regulator of the MAP-kinase signalling. Western blot analyses revealed that recombinant DUSP14 (rDUSP14) exists as the mixture of 22·5-kDa monomer and 45-kDa dimer under nonreducing conditions, and monomers under reducing conditions. Treatment with rDUSP14 at 4 °C for 2 h suppressed the ability of effector cells to transfer CHS dose dependently and the APC function of DLNCs to induce CHS. Epicutaneous application of rDUSP14 immediately after challenge inhibited the subsequent CHS expression. rDUSP14 was bound specifically by major histocompatibility complex class II (Ia)-positive spleen cells (presumably DCs). The suppressor activity of NSF was neutralized by anti-DUSP14 monoclonal antibody. Expression of DUSP14 mRNA in the spleen was upregulated parallel to the unresponsive state induced by hapten-conjugated cells. NSF, NSFint and rDUSP14 exhibited the phosphatase activity towards p -nitrophenyl phosphate in vitro as alkaline phosphatase. Conclusions, These studies indicate for the first time that NSF is a dimer of DUSP14 secreted by macrophage-like suppressor cells by stimulation with hapten-conjugated cells and exerts a regulatory function on CHS through DCs as a secreted phosphatase. [source] | |||||||||||||