Nanoparticle based Flu vaccine shows promise in pig study

An Ohio research group tested the efficacy of inactivated Swine Influenza virus (SwlV) encapsulated in 200–300 nm diameter PLGA (poly lactic co-glycolic acid) microspheres. Pigs were immunized twice intranasaly.  While control pigs had fever for four days, treated pigs showed no clinical flu symptoms.  “Biodegradable nanoparticle delivery of inactivated swine influenza virus vaccine provides heterologous […]

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Ancell anti-CD28 superagonist mAb used to expand Treg cells

“Single CD28 stimulation induces stable and polyclonal expansion of human regulatory T cells” Xuehui He, Ruben L Smeets,  Esther van Rijssen, Annemieke MH Boots, Irma Joosten, Hans JPM Koenen.  (2016) Dissertation Submitted for Publication,  Radbound Univ Med Center and Groningen Univ Med Center, The Netherlands. Ancell anti-CD28 Superagonist  Clone ANC28.1/5D10

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anti-CD32 F(ab’)2 blocked receptors on SLE patient-derived stimulated monocytes and reduced proinflammatory cytokine secretion in vitro

Macrophages derived in culture from SLE patients are directed into secreting proinflammatory cytokines by anti-C1q auto antibodies bound to immobilized C1q complement protein. Pre blocking these monocytes with anti-CD32 (FcgRII ) F(ab’)2 reduced cytokine secretion levels significantly. “Anti-C1q Autoantibodies from Systemic Lupus Erythematosus Patients Induce a Proinflammatory Phenotype in Macrophages.”  Sophia Thanei, Marten Trendelenburg  J

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TALEN gene editing used to restore normal CD154 expression and function in X-HIGM human T cells

Using TALEN(Transcription Activator-Like Effector Nucleases) technology, these researchers from Seattle Children’s Research succeeded in restoring copies of CD154( CD40L) gene with 3’ UTR under control of its endogenous promoter in human T cells from a patient with X-Linked Hyper-IgM Syndrome (X-HIGM). “Targeted gene editing restores regulated CD40L expression and function in X-HIGM T cells.” N

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Oxidized Mitochondrial products in NETosis are a major component by which LDG drive inflammation in SLE

Neutrophil Extracellular Trap (NET) is a mechanism by which bacteria and other pathogenic organisms are rendered trapped in a site of inflammation.  An activated Neutrophil extrudes it own genomic DNA, rich with histones and other proteins, to trap invading pathogenic organisms.  However, in SLE patients, a distinct subset of Neutrophils, Low Density Granulocytes (LDGs) are

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