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Passive Immunization (passive + immunization)
Selected AbstractsPassive immunization against oral AIDS virus transmission: An approach to prevent mother-to-infant HIV-1 transmission?JOURNAL OF MEDICAL PRIMATOLOGY, Issue 4 2001Regina Hofmann-Lehmann To develop immunoprophylaxis regimens against mother-to-child human immunodeficiency virus type 1 (HIV-1) transmission, we established a simian,human immunodeficiency virus (SHIV) model in neonatal macaques that mimics intrapartum mucosal virus exposure (T.W. Baba, J. Koch, E.S. Mittler et al.: AIDS Res Hum Retroviruses 10:351,357, 1994). We protected four neonates from oral SHIV-vpu+ challenge by ante- and postpartum treatment with a synergistic triple combination of immunoglobulin (Ig) G1 human anti-HIV-1 neutralizing monoclonal antibodies (mAbs) (T.W. Baba, V. Liska, R. Hofmann-Lehmann et al.: Nature Med 6:200,206, 2000), which recognize the CD4-binding site of Env, a glycosylation-dependent gp120, or a linear gp41 epitope. Two neonates that received only postpartum mAbs were also protected from oral SHIV-vpu+ challenge, indicating that postpartum treatment alone is sufficient. Next, we evaluated a similar mAb combination against SHIV89.6P, which encodes env of primary HIV89.6. One of four mAb-treated neonates was protected from infection and two maintained normal CD4+ T-cell counts. We conclude that the epitopes recognized by the three mAbs are important determinants for achieving protection. Combination immunoprophylaxis with synergistic mAbs seems promising to prevent maternal HIV-1 transmission in humans. [source] Antibodies against ,-amyloid reduce a, oligomers, glycogen synthase kinase-3, activation and , phosphorylation in vivo and in vitroJOURNAL OF NEUROSCIENCE RESEARCH, Issue 3 2006Qiu-Lan Ma Abstract Although active and passive immunization against the ,-amyloid peptide (A,) of amyloid plaque-bearing transgenic mice markedly reduces amyloid plaque deposition and improves cognition, the mechanisms of neuroprotection and impact on toxic oligomer species are not understood. We demonstrate that compared to control IgG2b, passive immunization with intracerebroventricular (icv) anti-A, (1,15) antibody into the AD HuAPPsw (Tg2576) transgenic mouse model reduced specific oligomeric forms of A,, including the dodecamers that correlate with cognitive decline. Interestingly, the reduction of soluble A, oligomers, but not insoluble A,, significantly correlated with reduced , phosphorylation by glycogen synthase kinase-3, (GSK-3,), a major , kinase implicated previously in mediating A, toxicity. A conformationally-directed antibody against amyloid oligomers (larger than tetramer) also reduced A, oligomer-induced activation of GSK3, and protected human neuronal SH-SY5Y cells from A, oligomer-induced neurotoxicity, supporting a role for A, oligomers in human , kinase activation. These data suggest that antibodies that are highly specific for toxic oligomer subspecies may reduce toxicity via reduction of GSK-3,, which could be an important strategy for Alzheimer's disease (AD) therapeutics. © 2005 Wiley-Liss, Inc. [source] Autoantibodies against ,-amyloid are common in Alzheimer's disease and help control plaque burden,ANNALS OF NEUROLOGY, Issue 1 2009Alexander Kellner MSc Objective Active or passive immunization of Alzheimer's disease (AD) patients leads to targeting of ,-amyloid plaques by immunoglobulins (IgG) and their subsequent removal by microglia. Here, we investigate whether naturally occurring autoantibodies to ,-amyloid contribute to ,-amyloid plaque removal in nonimmunized AD patients. Methods We generated an AD tissue microarray with 2,325 tissue specimens from 3 defined central nervous system regions of 48 AD patients and 48 age-matched control patients. Absolute quantification of ,-amyloid, ,-amyloid plaque-bound IgG, and phagocytic, resting, and activated microglia and microhemorrhages was done using a standardized, highly reproducible scoring system. Results The majority of neuritic plaques are decorated by IgG. AD patients with prominently IgG-labeled neuritic plaques have a significantly reduced plaque burden and an increase in phagocytic microglia, yet no increase in microhemorrhages. Interpretation Autoantibodies directed against ,-amyloid are common in AD patients and may contribute in controlling plaque burden. Ann Neurol 2009;65:24,31 [source] Biodistribution of liposome-entrapped human gamma-globulinBIOPHARMACEUTICS AND DRUG DISPOSITION, Issue 6 2006María A. García-Santana Abstract The present study was aimed at the preparation and performance evaluation of Intacglobin® -loaded liposomes for selective drug presentation to the lungs. Egg phosphatidylcholine- and cholesterol-based liposomes (1:1 and 1:0.25 mol/mol) were prepared by a dehydration,rehydration procedure. A tissue distribution study after single intranasal administration of 0.5 µCi 125I-Intacglobin® -loaded liposomes was conducted in Balb/c mice. The efficiencies of drug entrapment (30%) and the average diameters did not differ significantly between the two liposome formulations. However, liposomes composed of an increased cholesterol amount showed a lower in vitro drug release rate. The airway penetration efficiency of the liposomal formulation was determined by the cumulative percentage of the dose reaching the lungs (AUC) and its sojourn time therein, and were 1.7- and 2.2-times higher compared with the plain 125I- Intacglobin® solution-based formulation, respectively. A significantly greater (p<0.001) drug localization index after 24 h was found at the lungs in comparison with the other tissues (p<0.01), although similar values were detected between groups following administration of either liposomes or control solutions, despite the formulations attributes. In conclusion, it is suggested that longer Intacglobin exposure at the pulmonary region is observed after administration of the liposomal formulation. The results open future perspectives in assessing local passive immunization for the treatment of respiratory infectious diseases. Copyright © 2006 John Wiley & Sons, Ltd. [source] Cyclosporin A inhibits eosinophilic infiltration into the conjunctiva mediated by type IV allergic reactionsCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 4 2006Atsuki Fukushima MD Abstract Background:, Eosinophils are important effector cells in severe allergic conjunctivitis such as vernal keratoconjunctivitis. Infiltration of eosinophils into the conjunctiva is mediated by type I and type IV allergic reactions. Cyclosporin A (CsA) eye drops are administered therapeutically for severe allergic conjunctivitis, but the mechanism by which CsA acts, that is, by inhibiting type I, type IV or both types of allergic reactions, is not known. We investigated whether CsA eye drops inhibit type I, type IV or both types of allergic reactions in the conjunctiva. Methods:, Experimental immune-mediated blepharoconjunctivitis (EC) was induced in BALB/c mice by either active immunization or passive immunization by transfer of ragweed (RW)-primed splenocytes and RW-specific IgE, followed by RW challenge to the conjunctiva. These mice were treated in eye drops with vehicle, 0.1% CsA, 0.5% CsA or 0.1% betamethasone five times (1 and 2 h before RW challenge and 1, 2 and 3 h after RW challenge). Twenty-four hours after the challenge, the conjunctivas were harvested for histological analysis to evaluate eosinophilic infiltration. To evaluate effects of CsA eye drops on systemic immune responses, sera and spleens were collected from actively immunized mice at the time of sacrifice to examine serum IgE levels and cellular immune responses, respectively. Results:, CsA eye drops significantly inhibited eosinophilic infiltration into the conjunctiva in actively immunized EC-developing mice compared with vehicle-treated mice. The CsA-induced inhibition was similar to inhibition induced by 0.1% betamethasone. Serum IgE levels and splenocyte responses in CsA-treated mice were equivalent to those in vehicle-treated mice. Betamethasone treatment inhibited eosinophilic infiltration into the conjunctiva induced by both splenocyte transfer and IgE transfer, while CsA treatment inhibited infiltration induced by splenocyte transfer. Conclusions:, CsA eye drops inhibited eosinophilic infiltration into the conjunctiva without affecting systemic immune responses. CsA predominantly inhibits eosinophilic infiltration by interfering with the type IV allergic reaction in the conjunctiva. [source] | ||||||||||