Abstract: The embodiment of the invention is to enable universal non-classical MHC I peptide vaccines restricted to HLA-E, HLA-F and HLA-G. An algorithm was develop to predict HLA-E binding immunogenic or suppressorgenic peptides of the autologous origins, e.g., autoantigens, inflammatory antigens, IgE and cancer antigens, and of the microbial origins. Thus, the embodiment of the invention is to load the antigenic peptides of medical and therapeutic importance onto the non-polymorphic HLA-E, HLA-F, and HLA-G culminating in universal vaccines, bypassing highly polymorphic classical MHC I, e.g., HLA-A, HLA-B and HLA-C pathways, in order to treat autoimmune diseases, allergy, inflammatory diseases, cancers, and infectious diseases for all human population. Derlin-1 and UL40 pathways are utilized to enable antigen presentation and vaccine efficacies in the non-classical MHC I pathways.

Abstract: The embodiment of the invention is to innovate immunogenic CoV-2, CoV-n B cell epitopes, which are selected from the loop regions constrained by the two constraining beta strands; or between one beta strand and one alpha-helical strand; or between two alpha-helical strands of CoV-2, CoV-n proteins, and such selected loops replace the native loops of the thermostable protein scaffolds, which provide thermostable constraint of the transplanted CoV-2, CoV-n loop antigens as well as CD4 helper T cell determinants to elicit CD4 dependent neutralizing and blocking antibodies against viral entry, replication and viral clearance. The B cell loops can be cleaved and processed as CD8 T cell epitopes for eliciting cytotoxic T lymphocyte (CTL) responses against and clear viral infected cells. MHCI viral peptide epitopes in nonamers, octamers, or decamers will be used as peptide vaccines along with viral CD4 helper peptide epitopes.

Abstract: Galectin-3 is a pro-inflammatory molecule functioning as a cytokine hub, and also regulates unfolded protein responses (UPR) and ER stress. Thus, galectin-3 serves as a target for ameliorating inflammatory diseases such as allergic inflammation and diabetic inflammation and insulin resistance. RNA interference of endogenous galectin-3 expression, upregulates IL-12, IL-10 while downregulating IL-23 production, which offers protection against allergic inflammation. In addition, endogenous galectin-3 knockdown causes upregulation of XBP1, alleviating ER stress. Together, upregulated XBP1 and IL-10 offer protection against obesity-induced inflammation. Therefore, the embodiment of the invention resides in RNA interference of endogenous galectin-3 in appropriate cell types in order to rectify allergic and/or diabetic inflammation.

Abstract: The embodiment of the invention is to enable universal non-classical MHC I peptide vaccines restricted to HLA-E, HLA-F and HLA-G. An algorithm was develop to predict HLA-E binding immunogenic or suppressorgenic peptides of the autologous origins, e.g., autoantigens, inflammatory antigens, IgE and cancer antigens, and of the microbial origins. Thus, the embodiment of the invention is to load the antigenic peptides of medical and therapeutic importance onto the non-polymorphic HLA-E, HLA-F, and HLA-G culminating in universal vaccines, bypassing highly polymorphic classical MHC I, e.g., HLA-A, HLA-B and HLA-C pathways, in order to treat autoimmune diseases, allergy, inflammatory diseases, cancers, and infectious diseases for all human population. Derlin-1 and UL40 pathways are utilized to enable antigen presentation and vaccine efficacies in the non-classical MHC I pathways.

Abstract: Galectin-3 is a pro-inflammatory molecule functioning as a cytokine hub, and also regulates unfolded protein responses (UPR) and ER stress. Thus, galectin-3 serves as a target for ameliorating inflammatory diseases such as allergic inflammation and diabetic inflammation and insulin resistance. RNA interference of endogenous galectin-3 expression, upregulates IL-12, IL-10 while downregulating IL-23 production, which offers protection against allergic inflammation. In addition, endogenous galectin-3 knockdown causes upregulation of XBP1, alleviating ER stress. Together, upregulated XBP1 and IL-10 offer protection against obesity-induced inflammation. Therefore, the embodiment of the invention resides in RNA interference of endogenous galectin-3 in appropriate cell types in order to rectify allergic and/or diabetic inflammation.