Abstract: Embodiments of the invention related generally to the treatment or prevention of infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and, more particularly, to the use of (S)-crizotinib or a pharmaceutically-acceptable salt thereof in such treatment or prevention. In one embodiment, the invention provides a method of treating a patient diagnosed with SARS-CoV-2, the method comprising: administering to the patient a dose of (S)-crizotinib or a pharmaceutically-acceptable salt thereof.

Abstract: This invention relates to methods of expanding T regulatory cells through OX40L and Jagged-1 induced signaling. The methods can be used for treating autoimmune diseases.

Abstract: Compositions and methods for treating cancers are provided which comprise administering a combination of antineoplastic agents, wherein the combination comprises protein kinase inhibitor, anthracycline, nucleoside analog, apoptosis-inducing molecular therapeutic or alkylating agent chemotherapeutics and one or more nucleic acid molecules capable of down-regulating expression of at least one splice variant of the IG20 gene, and wherein not all splice variants of the IG20 gene are down-regulated. Preferably, the splice variant of the IG20 gene is a MADD splice variant and the nucleic acid molecules are siRNA, shRNA and antisense oligonucleotides which comprise a nucleic acid sequence complementary to a nucleic acid sequence of exon 13L of the MADD splice variant or to an mRNA transcript of exon 13L of the MADD splice variant.

Abstract: This invention relates to methods of expanding T regulatory cells through OX40L and Jagged-1 induced signaling. The methods can be used for treating autoimmune diseases.

Abstract: This invention relates to methods of expanding T regulatory cells through OX40L and Jagged-1 induced signaling. The methods can be used for treating autoimmune diseases.

Abstract: Compositions and methods for treating cancers are provided which comprise administering a combination of antineoplastic agents, wherein the combination comprises protein kinase inhibitor, anthracycline, nucleoside analog, apoptosis-inducing molecular therapeutic or alkylating agent chemotherapeutics and one or more nucleic acid molecules capable of down-regulating expression of at least one splice variant of the IG20 gene, and wherein not all splice variants of the IG20 gene are down-regulated. Preferably, the splice variant of the IG20 gene is a MADD splice variant and the nucleic acid molecules are siRNA, shRNA and antisense oligonucleotides which comprise a nucleic acid sequence complementary to a nucleic acid sequence of exon 13L of the MADD splice variant or to an mRNA transcript of exon 13L of the MADD splice variant.

Abstract: This invention relates to methods of expanding T regulatory cells through OX40L and Jagged-1 induced signaling. The methods can be used for treating autoimmune diseases.

Abstract: This invention relates to methods of expanding T regulatory cells through OX40L and Jagged-1 induced signaling. The methods can be used for treating autoimmune diseases.

Abstract: GM-CSF administered before immunization exerted a sustained suppressive effect against the induction of myasthenia gravis (MG). This suppression was associated with lowered serum autoantibody levels, reduced T cell proliferative responses to AChR, and an expansion in the population of FoxP3+ regulatory T cells. Manipulating DCs to expand regulatory T cells is useful for the control of autoimmune diseases such as myasthenia gravis MG.