Methods and products for diagnosing, treating and/or delaying onset of chronic allograft rejection, including cardiac allograft vasculopathy. In an exemplary embodiment of a noninvasive method of screening a cardiac allograft recipient for being at-risk for developing cardiac allograft vasculopathy of the present disclosure, the method comprises the steps of withdrawing at least one biological sample from a cardiac allograft recipient; and analyzing the at least one biological sample for one or more biomarkers indicative of the presence of fibrin deposits within the cardiac allograft microvasculature; wherein detection of the one or more biomarkers indicates that the cardiac allograft recipient is at-risk for or developing cardiac allograft vasculopathy.

Compositions and methods for modified dendrimer nanoparticle (“MDNP”) delivery of therapeutic, prophylactic and/or diagnostic agent such as large repRNA molecules to the cells of a subject have been developed. MDNPs efficiently drive proliferation of antigen-specific T cells against intracellular antigen, and potentiate antigen-specific antibody responses. MDNPs can be multiplexed to deliver two or more different repRNAs to modify expression kinetics of encoded antigens and to simultaneous deliver repRNAs and mRNAs including the same UTR elements that promote expression of encoded antigens.

Fusion protein nanodisk compositions and methods of treating a variety of disorders by administration of the fusion protein nanodisk compositions to a patient in need are disclosed. The fusion protein nanodisks provide for the combined delivery of two different apolipoproteins to a subject in need. Fusion protein nanodiscs may include a phospholipid bilayer encompassed by a fusion membrane scaffold protein. The fusion membrane scaffold protein may include two different amphipathic alpha-helical proteins, such as apolipoproteins. Methods for treating a disorder by administering a therapeutic amount of the fusion protein nanodisc described above are also disclosed.

The invention relates to multiple epitope constructs, immunogenic and vaccine compositions comprising recombinant molecules presenting inserted multiple and different epitopes from a variety of antigens. The antigenic determinants being associated with different pathways leading to atherosclerosis. In particular, the invention relates to such compositions for eliciting an immune response against antigens and pathogens involved in the development of atherosclerosis. The invention includes inter alia methods of treating and/or preventing the disease and recombinant protein products.

The invention relates to a virus like particle (VLP) based vaccine. The virus-like particle constitutes a non-naturally occurring, ordered and repetitive antigen array display scaffold which can obtain a strong and long-lasting immune response in a subject. The VLP based vaccine may be used for the prophylaxis and/or treatment of a disease including, but is not limited to, cancer, cardiovascular, infectious, asthma, and/or allergy diseases/disorders.

Methods and products for diagnosing, treating and/or delaying onset of chronic allograft rejection, including cardiac allograft vasculopathy. In an exemplary embodiment of a noninvasive method of screening a cardiac allograft recipient for being at-risk for developing cardiac allograft vasculopathy of the present disclosure, the method comprises the steps of withdrawing at least one biological sample from a cardiac allograft recipient; and analyzing the at least one biological sample for one or more biomarkers indicative of the presence of fibrin deposits within the cardiac allograft microvasculature; wherein detection of the one or more biomarkers indicates that the cardiac allograft recipient is at-risk for or developing cardiac allograft vasculopathy.

Provided are compositions and methods for using the same. In some embodiments, the compositions include an EPELN encapsulating and/or having associated therewith an active agent and a plasma membrane derived from a tumor and/or cancer cell coating the EPELN. In some embodiments, the active agent is a therapeutic agent or an immune response modifier, and in some embodiments the plasma membrane has one or more tumor-associated and/or cancer-associated antigens. Also provided are methods for using the compositions for treating tumors and/or cancers, inducing anti-tumor and/or anti-cancer immune responses, activating antigen-presenting cells, targeting CD1 lc dendritic cells, and preventing or reducing metastasis.

Disclosed herein are vectors that include antigen-encoding nucleic acid sequences and co-express immune modulators. Also disclosed are nucleotides, cells, and methods associated with the vectors including their use as vaccines.

An immunogen generally includes a virus-like particle and an antigen linked to the virus-like particle. The antigen includes an antigenic portion of a polypeptide, wherein the polypeptide inhibits lipoprotein lipase (LPL) activity by binding to LPL. In some embodiments, the polypeptide is at least a portion of angiopoietin-like 3 (ANGPTL3). In other embodiments, the polypeptide is at least a portion of angiopoietin-like 4 (ANGPTL4). In other embodiments, the polypeptide at least a portion of angiopoietin-like 8 (ANGPTL8). In some embodiments, the virus-like particle is a Qbeta immunogenic carrier. In some of these embodiments, the antigen is linked to the virus-like particle through a Gly-Gly-Gly-Cys linker at the C-terminal of the antigen.

The invention relates to therapeutic nanobiologic compositions and methods of treating patients who have had an organ transplant, or who suffer from atherosclerosis, arthritis, inflammatory bowel disease including Crohn's, autoimmune diseases including diabetes, and/or autoinflammatory conditions, or after a cardiovascular events, including stroke and myocardial infarction, by inhibiting trained immunity, which is the long-term increased responsiveness, the result of metabolic and epigenetic re-wiring of myeloid cells and their stem cells and progenitors in the bone marrow and spleen and blood induced by a primary insult, and characterized by increased cytokine excretion after re-stimulation with one or multiple secondary stimuli.