This disclosure relates to acellular-based therapies for modulating the level of regulatory T cells (Treg) and/or the level of pro-inflammatory T cells (Th17/Th1). To provide these therapeutic effects, a combination comprising at least one acellular pro-tolerogenic preparation and at least one acellular pro-inflammatory preparation are administered sequentially.

Synthetic molecule construct of the structure F-S.sub.1-S.sub.2-L where FS.sub.1 is an aminoalkylglycoside and S.sub.2-L is a dicarboxylated, e.g. adipylated, phosphatidylethanolamide are disclosed. The two terminal sugars of the aminoalkylglycoside (Gal1-3Gal-) are the two terminal sugars of the Galili antigen.

The present invention provides compositions and methods for inducing antigen-specific tolerance in a subject. In one embodiment, the present invention provides a composition comprising an apoptotic body and an epitope of an antigen. Also provided herein are methods of preparing and administering the composition. The composition and methods provided herein can induce antigen-specific tolerance in a subject.

The present disclosure provides methods and systems for cell and bead processing or analysis. A method for processing a cell or bead may comprise subjecting a bead to conditions sufficient to change a first characteristic or set of characteristics (e.g., cell or bead size). Such a method may further comprise subjecting the cell or bead to conditions sufficient to change a second characteristic or set of characteristics. In some cases, crosslinks may be formed within the cell or bead.

Provided herein are engineered cells, comprising: a chemical or biological moiety covalently bound to a cell surface glycan, wherein the chemical or biological moiety is selected from the group consisting of small molecule, polynucleotide, polypeptide, and antibody. Also provided are compositions comprising these engineered cells and methods of making and using the same.

Vacuole- or exosome-inducing indole-based chalcone and substituted triazole-hydrazone compounds that induce endosomal vacuolization and increase exosome yield, but do not trigger growth arrest or cell death, and methods of making and using are described.

Normal or genetically modified cell(s) having magnetic nanoparticle(s) bound (affixed) to their surfaces and methods of delivery to target tissues, e.g. for treatment of disease and/or injury.

The present invention relates to processes and systems for preparing nanoparticles, cellular or viral membranes and/or cellular or viral membrane coated nanoparticles using or comprising, inter alia, a multi-inlet vortexing reactor, tangential flow filtration (TFF) and/or a high shear fluid processor such as a microfluidizer (or a microfluidizer processor). The present invention also relates to the nanoparticles, cellular or viral membranes and/or cellular or viral membrane coated nanoparticles prepared by the present processes and systems, and the uses and/or applications of the nanoparticles, cellular or viral membranes and/or cellular or viral membrane coated nanoparticles.

A cell treatment agent contains at least one selected from the group consisting of alginic acid, heparins, dextran sulfate, and a proteolytic enzyme inhibitor, as an effective component.

The invention provides engineered mitochondria and a preparation method thereof, and relates to the technical field of mitochondria. The engineered mitochondria are formed by attaching exogenous cell membranes to outer membranes of exogenous mitochondria. The preparation method comprises the following steps: S1: extracting exogenous cell membranes from cells; S2: separating and extracting exogenous mitochondria from cells or tissue; and S3: mixing the separated and extracted exogenous mitochondria with the exogenous cell membranes in a specific ratio, thereby attaching the exogenous cell membranes to the outer membranes of the exogenous mitochondria to obtain the engineered mitochondria. The invention enables the production of engineered mitochondria with enhanced biological activity, exhibiting improved therapeutic effects on mitochondrial dysfunction-related disorders.