Abstract: Small molecule AhR ligands are disclosed. The ligands can induce the differentiation of Tr1 cells to suppress pathogenic immune responses without inducing nonspecific immune suppression. Methods of treatment of autoimmune diseases using the AhR ligands are also disclosed.

Abstract: A composition and method for treating autoimmune disease includes administering an effective amount of an aryl hydrocarbon receptor (AhR) ligand. The AhR ligand includes 11-Cl-BBQ, 10-Cl-BBQ, an analog of 11-Cl-BBQ, or combination thereof. The AhR ligand is administered topically, orally, transdermally, intravenously, subcutaneously, or with a nanoparticle. The AhR ligand induces regulatory T cells (AhR-Tregs). AhR-Treg cells block the differentiation of cytotoxic T-lymphocytes (CTL). The AhR ligand activates AhR in CD4+ T cells to induce CD4+ AhR-Tregs that suppress the development of effector CTL, thereby suppressing the development of CTL that attack host cells in graft versus host disease (GVHD) or ?-cells in the pancreas in diabetes mellitus type 1 (T1DM). The AhR ligand can also suppress development of CTL independently of Foxp3+ regulatory T cell induction. The AhR ligand can therefore be used to treat autoimmune diseases characterized by an absence of functional Foxp3+ regulatory T cell.

Abstract: A composition and method for treating autoimmune disease includes administering an effective amount of an aryl hydrocarbon receptor (AhR) ligand. The AhR ligand includes 11-Cl-BBQ, 10-Cl-BBQ, an analog of 11-Cl-BBQ, or combination thereof. The AhR ligand is administered topically, orally, transdermally, intravenously, subcutaneously, or with a nanoparticle. The AhR ligand induces regulatory T cells (AhR-Tregs). AhR-Treg cells block the differentiation of cytotoxic T-lymphocytes (CTL). The AhR ligand activates AhR in CD4+ T cells to induce CD4+ AhR-Tregs that suppress the development of effector CTL, thereby suppressing the development of CTL that attack host cells in graft versus host disease (GVHD) or ?-cells in the pancreas in diabetes mellitus type 1 (T1DM). The AhR ligand can also suppress development of CTL independently of Foxp3+ regulatory T cell induction. The AhR ligand can therefore be used to treat autoimmune diseases characterized by an absence of functional Foxp3+ regulatory T cell.

Abstract: Compounds that modulate the function of anti-apoptotic proteins such as Bcl-2 and Bcl-XL are identified. These compounds have the ability to convert the activity of Bcl-2-family member proteins from anti-apoptotic to pro-apoptotic. Methods for inducing apoptosis are described, together with methods for identifying molecules that induce apoptosis through interaction with Bcl-2-family members.

Abstract: Compounds that modulate the function of anti-apoptotic proteins such as Bcl-2 and Bcl-XL are identified. These compounds have the ability to convert the activity of Bcl-2-family member proteins from anti-apoptotic to pro-apoptotic. Methods for inducing apoptosis are described, together with methods for identifying molecules that induce apoptosis through interaction with Bcl-2-family members.

Abstract: Compounds that modulate the function of anti-apoptotic proteins such as Bcl-2 and Bcl-XL are identified. These compounds have the ability to convert the activity of Bcl-2-family member proteins from anti-apoptotic to pro-apoptotic. Methods for inducing apoptosis are described, together with methods for identifying molecules that induce apoptosis through interaction with Bcl-2-family members.

Abstract: Compounds that modulate the function of anti-apoptotic proteins such as Bcl-2 and Bcl-XL are identified. These compounds have the ability to convert the activity of Bcl-2-family member proteins from anti-apoptotic to pro-apoptotic. Methods for inducing apoptosis are described, together with methods for identifying molecules that induce apoptosis through interaction with Bcl-2-family members.

Abstract: Compounds that modulate the function of anti-apoptotic proteins such as Bcl-2 and Bcl-XL are identified. These compounds have the ability to convert the activity of Bcl-2-family member proteins from anti-apoptotic to pro-apoptotic. Methods for inducing apoptosis are described, together with methods for identifying molecules that induce apoptosis through interaction with Bcl-2-family members.

Abstract: Compounds that modulate the function of anti-apoptotic proteins such as Bcl-2 and Bcl-XL are identified. These compounds have the ability to convert the activity of Bcl-2-family member proteins from anti-apoptotic to pro-apoptotic. Methods for inducing apoptosis are described, together with methods for identifying molecules that induce apoptosis through interaction with Bcl-2-family members.

Abstract: The invention relates to a process for preparing agents which are suitable for treating tumour diseases or for immunosuppression, with target cells being treated with chemical compounds which bind to the Ah receptor of the target cells, the binding of the chemical compound(s) to the Ah receptor of the target cells being determined by measuring the expression, which is induced thereby, of a detector gene which is relevant for the effects of the chemical compound(s), and the chemical compound(s) which has/have been found in this way being used for preparing the agent(s).