Abstract: The present disclosure is directed to a method for treating an autoimmune disease, the method comprising administering to a subject in need thereof a cannabinoid compound comprising delta-8-tetrahydrocannabinol.

Abstract: The present disclosure is directed to compositions and methods to treat the inflammatory response present in certain diseases and illnesses by modifying a dysregulation of one or more genes associated with the Wnt/?-catenin signaling pathway. Embodiments of the disclosure can provide methods for treating an inflammatory response in a patient by identifying the inflammatory response and modifying the inflammatory response.

Abstract: The present disclosure is directed to compositions and methods for treating obesity or an inflammatory state present in obese mammals. In general, the methods and compositions disclosed herein utilize previously unrecognized miR regulatory pathways to reduce pro-inflammatory cytokine secretion and promote egress of immune cells from inflammation sites. An example aspect of the present disclosure includes methods for treating obesity or an inflammatory state in a mammal, the method including delivering a cannabinoid receptor 1 antagonist, a Netrin-1 inhibitor, a miR inhibitor, a miR, a miR mimic, or combinations thereof to the mammal.

Abstract: The present application relates to induction of a Treg phenotype in mammalian naïve CD4+ T cells. In certain embodiments, the methods and compositions described can be applied as methods to treat autoimmune disorders or transplant complications (e.g., lupus and graft-versus-host disease) and may be used in combination with, but do not require, systemic immune suppression, such as a chemotherapeutic agent. In particular, embodiments of the disclosure can utilize transforming growth factor-beta 2 (TGFB2), molecules that stimulate the production of TGFB2, inhibitors of molecules that suppress production of TGFB2, or molecules that effect the function of TGFB2 to induce a Treg phenotype in naïve CD4+ T cells from a mammal. Provided herein are embodiments and examples demonstrating the production of Treg cells, as well as the application of Treg cells in modulating the inflammatory response present in certain diseases.

Abstract: Described herein are functional CB1 signaling in immune cells is necessary to dampen HFD-induced microglia/macrophage-mediated neuroinflammation and reduce obesity, targeting immune CB1 receptors constitutes a novel therapeutic modality to lessen Diet-Induced Obesity, and circumvent adverse side effects of CB1 antagonist or neuronal CB1 agonist treatment.

Abstract: The present disclosure is directed to compositions and methods for treating obesity or an inflammatory state present in obese mammals. In general, the methods and compositions disclosed herein utilize previously unrecognized miR regulatory pathways to reduce pro-inflammatory cytokine secretion and promote egress of immune cells from inflammation sites. An example aspect of the present disclosure includes methods for treating obesity or an inflammatory state in a mammal, the method including delivering a cannabinoid receptor 1 antagonist, a Netrin-1 inhibitor, a miR inhibitor, a miR, a miR mimic, or combinations thereof to the mammal.

Abstract: The present application relates to induction of a Treg phenotype in mammalian naïve CD4+ T cells. In certain embodiments, the methods and compositions described can be applied as methods to treat autoimmune disorders or transplant complications (e.g., lupus and graft-versus-host disease) and may be used in combination with, but do not require, systemic immune suppression, such as a chemotherapeutic agent. In particular, embodiments of the disclosure can utilize transforming growth factor-beta 2 (TGFB2), molecules that stimulate the production of TGFB2, inhibitors of molecules that suppress production of TGFB2, or molecules that effect the function of TGFB2 to induce a Treg phenotype in naïve CD4+ T cells from a mammal. Provided herein are embodiments and examples demonstrating the production of Treg cells, as well as the application of Treg cells in modulating the inflammatory response present in certain diseases.

Abstract: The present disclosure is directed to compositions and methods to treat the inflammatory response present in certain diseases and illnesses by modifying a dysregulation of one or more genes associated with the Wnt/?-catenin signaling pathway. Embodiments of the disclosure can provide methods for treating an inflammatory response in a patient by identifying the inflammatory response and modifying the inflammatory response.

Abstract: MicroRNA-30 is identified as being dysregulated in adipose tissue macrophages during obesity and can be used in treatment of disease in which adipose tissue macrophage polarization dysregulation plays a part. Increased concentration of microRNA-30, e.g., via pharmaceutical delivery, can decrease the polarization of macrophages, and in particular adipose tissue macrophages, to inflammatory M1 phenotype and can decrease expression of pro-inflammatory cytokines. One or more members of the miR-30 family can be utilized in the methods. Methods can be beneficial in treatment of a large number of inflammatory diseases including obesity, diabetes, cancer, autoimmune, etc.

Abstract: MicroRNA-30 is identified as being dysregulated in adipose tissue macrophages during obesity and can be used in treatment of disease in which adipose tissue macrophage polarization dysregulation plays a part. Increased concentration of microRNA-30, e.g., via pharmaceutical delivery, can decrease the polarization of macrophages, and in particular adipose tissue macrophages, to inflammatory M1 phenotype and can decrease expression of pro-inflammatory cytokines. One or more members of the miR-30 family can be utilized in the methods. Methods can be beneficial in treatment of a large number of inflammatory diseases including obesity, diabetes, cancer, autoimmune, etc.

Abstract: Methods for diagnosis and treatment of endometriosis are described. Methods utilize the recognition that leukocyte miRNAs can be dramatically dysregulated subjects suffering from endometriosis. Accordingly, leukocyte miRNAs, as well as polynucleotides encoding the miRNAs, can be utilized in the diagnosis and treatment of endometriosis.

Abstract: Methods for diagnosis and treatment of endornetriosis are described. Methods utilize the recognition that leukocyte miRNAs can be dramatically dysregulated subjects suffering from endometriosis. Accordingly, leukocyte miRNAs, as well as polynucleotides encoding the miRNAs, can be utilized in the diagnosis and treatment of endometriosis.

Abstract: Methods for diagnosis and treatment of endometriosis are described. Methods utilize the recognition that leukocyte miRNAs can be dramatically dysregulated subjects suffering from endometriosis. Accordingly, leukocyte miRNAs, as well as polynucleotides encoding the miRNAs, can be utilized in the diagnosis and treatment of endometriosis.

Abstract: Methods for diagnosis and treatment of endometriosis are described. Methods utilize the recognition that leukocyte miRNAs can be dramatically dysregulated subjects suffering from endometriosis. Accordingly, leukocyte miRNAs, as well as polynucleotides encoding the miRNAs can be utilized in the diagnosis and treatment of endometriosis.

Abstract: A method for detecting a predisposition to breast cancer in a subject is provided. The method includes detecting in a biological sample from the subject one or more polymorphisms in the sequence of CD44 gene. The presence of one or more polymorphisms in the sequence of CD44 gene indicates that the subject has a predisposition for developing breast cancer.

Abstract: A method for detecting a predisposition to breast cancer in a subject is provided. The method includes detecting in a biological sample from the subject one or more polymorphisms in the sequence of CD44 gene. The presence of one or more polymorphisms in the sequence of CD44 gene indicates that the subject has a predisposition for developing breast cancer.

Abstract: Cannabinoids are known to interact with CB1 and CB2 receptors expressed in the nervous and immune systems mediating a wide range of effects, including anti-inflammatory properties. However, cannabinoids that bind CB1 are also psychoactive thereby limiting their clinical use. Cannabidiol (CBD) is the most abundant nonpsychotropic plant cannabinoid but has not been studied as extensively as ?9-tetrahydrocannabinol (THC). The present disclosure reports the immunosuppressive properties of CBD and demonstrates that CBD induces apoptosis in thymocytes and splenocytes and inhibits the proliferative responsiveness of T and B cells. This indicates that CB2 selective agonists, devoid of psychotropic effect, may serve as novel anti-inflammatory/immunosuppressive agents.

Abstract: Methods of treating autoimmune hepatitis are provided. The methods include injecting cannabidiol into the subject, where the cannabidiol is synthetic cannabidiol or natural cannabidiol isolated from other natural cannabinoids.

Abstract: A method for detecting a predisposition to breast cancer in a subject is provided. The method comprises detecting in a biological sample from the subject one or more polymorphisms in the sequence of CD44 gene. The presence of one or more polymorphisms in the sequence of CD44 gene indicates that the subject has a predisposition for developing breast cancer.

Abstract: Cannabinoids are known to interact with CB1 and CB2 receptors expressed in the nervous and immune systems mediating a wide range of effects, including anti-inflammatory properties. However, cannabinoids that bind are also psychoactive thereby limiting their clinical use. Cannabidiol (CBD) is the most abundant nonpsychotropic plant cannabinoid but has not been studied as extensively as ?9-tetrahydrocannabinol (THC). The present disclosure reports the immunosuppressive properties of CBD and demonstrates that CBD induces apoptosis in thymocytes and splenocytes and inhibits the proliferative responsiveness of T and B cells. This indicates that CB2 selective agonists, devoid of psychotropic effect, may serve as novel anti-inflammatory/immunosuppressive agents.