Abstract: Methods of treating neuroinflammation in a subject by administering to the subject an agent that inhibits activation of coagulation factor XI (FXI), inhibits the activity of activated FXI (FXIa), or reduces expression of FXI are described. The agent that inhibits activation of FXI can be a monoclonal antibody specific for FXI, such as a monoclonal antibody having the complementarity determining region (CDR) sequences of anti-FXI antibody 14E11. Small molecule inhibitors and antisense compounds directed to FXI or FXIa are also contemplated as agents that inhibit activity of FXIa or reduce expression of FXI. The neuroinflammation in the subject can be associated with any one of a number of different diseases or disorders, such as an autoimmune disease of the central nervous system (CNS) or a neurodegenerative disease.

Abstract: Recombinant polypeptides comprising a modified DR?1 domain are provided. In some embodiments, the polypeptides include the modified DR?1 domain, an antigenic peptide, and optionally a linker sequence. Pharmaceutical compositions comprising the recombinant polypeptides, methods of treating inflammatory disease using said recombinant polypeptides or pharmaceutical compositions, and expression constructs comprising nucleic acids that encode the recombinant polypeptides are also provided.

Abstract: Recombinant polypeptides comprising a modified DR?1 domain are provided. In some embodiments, the polypeptides include the modified DR?1 domain, an antigenic peptide, and optionally a linker sequence. Pharmaceutical compositions comprising the recombinant polypeptides, methods of treating inflammatory disease using said recombinant polypeptides or pharmaceutical compositions, and expression constructs comprising nucleic acids that encode the recombinant polypeptides are also provided.

Abstract: Methods and compositions used in treating traumatic brain injury using a recombinant DR?-MOG-35-55 construct are disclosed. The disclosed methods involve administering a pharmaceutical composition comprising DR?-MOG-35-55 and a pharmaceutically acceptable carrier to a subject that has had a traumatic brain injury.

Abstract: Two-domain MHC polypeptides are useful for modulating activities of antigen-specific T-cells, including for modulating pathogenic potential and effects of antigen-specific T-cells. Exemplary MHC class II-based recombinant T-cell ligands (RTLs) of the invention include covalently linked ?1 and ?1 domains, and MHC class I-based molecules that comprise covalently linked ?1 and ?2 domains. These polypeptides may also include covalently linked antigenic determinants, toxic moieties, and/or detectable labels. The disclosed polypeptides can be used to target antigen-specific T-cells, and are useful, among other things, to detect and purify antigen-specific T-cells, to induce or activate T-cells, to modulate T-cell activity, including by regulatory switching of T-cell cytokine and adhesion molecule expression, to treat conditions mediated by antigen-specific T-cells, including treatment and/or prevention of central nervous system damage relating to stroke.

Abstract: Two-domain MHC polypeptides are useful for modulating activities of antigen-specific T-cells, including for modulating pathogenic potential and effects of antigen-specific T-cells. Exemplary MHC class II-based recombinant T-cell ligands (RTLs) of the invention include covalently linked ?1 and ?1 domains, and MHC class I-based molecules that comprise covalently linked ?1 and ?2 domains. These polypeptides may also include covalently linked antigenic determinants, toxic moieties, and/or detectable labels. The disclosed polypeptides can be used to target antigen-specific T-cells, and are useful, among other things, to detect and purify antigen-specific T-cells, to induce or activate T-cells, to modulate T-cell activity, including by regulatory switching of T-cell cytokine and adhesion molecule expression, to treat conditions mediated by antigen-specific T-cells, including treatment and/or prevention of central nervous system damage relating to stroke.

Abstract: Two-domain MHC polypeptides are useful for modulating activities of antigen-specific T-cells, including for modulating pathogenic potential and effects of antigen-specific T-cells. Exemplary MHC class II-based recombinant T-cell ligands (RTLs) of the invention include covalently linked ?1 and ?1 domains, and MHC class I-based molecules that comprise covalently linked ?1 and ?2 domains. These polypeptides may also include covalently linked antigenic determinants, toxic moieties, and/or detectable labels. The disclosed polypeptides can be used to target antigen-specific T-cells, and are useful, among other things, to detect and purify antigen-specific T-cells, to induce or activate T-cells, to modulate T-cell activity, including by regulatory switching of T-cell cytokine and adhesion molecule expression, to treat conditions mediated by antigen-specific T-cells, including treatment and/or prevention of central nervous system damage relating to stroke.

Abstract: Two-domain MHC polypeptides are useful for modulating activities of antigen-specific T-cells, including for modulating pathogenic potential and effects of antigen-specific T-cells. Exemplary MHC class II-based recombinant T-cell ligands (RTLs) of the invention include covalently linked ?1 and ?1 domains, and MHC class I-based molecules that comprise covalently linked ?1 and ?2 domains. These polypeptides may also include covalently linked antigenic determinants, toxic moieties, and/or detectable labels. The disclosed polypeptides can be used to target antigen-specific T-cells, and are useful, among other things, to detect and purify antigen-specific T-cells, to induce or activate T-cells, to modulate T-cell activity, including by regulatory switching of T-cell cytokine and adhesion molecule expression, to treat conditions mediated by antigen-specific T-cells, including treatment and/or prevention of central nervous system damage relating to stroke.

Abstract: Two-domain MHC polypeptides are useful for modulating activities of antigen-specific T-cells, including for modulating pathogenic potential and effects of antigen-specific T-cells. Exemplary MHC class II-based recombinant T-cell ligands (RTLs) of the invention include covalently linked ?1 and ?1 domains, and MHC class I-based molecules that comprise covalently linked ?1 and ?2 domains. These polypeptides may also include covalently linked antigenic determinants, toxic moieties, and/or detectable labels. The disclosed polypeptides can be used to target antigen-specific T-cells, and are useful, among other things, to detect and purify antigen-specific T-cells, to induce or activate T-cells, to modulate T-cell activity, including by regulatory switching of T-cell cytokine and adhesion molecule expression, to treat conditions mediated by antigen-specific T-cells, including treatment and/or prevention of central nervous system damage relating to stroke.

Abstract: The present disclosure relates to methods for inhibiting an autoimmune disease by administering to a subject a therapeutically effective amount of a composition that increases FOXP3 expression, thereby inhibiting the autoimmune disease. Further disclosed herein are methods for detecting in a subject an autoimmune disease or a predisposition to an autoimmune disease, and methods for assessing the efficacy of a therapy for an autoimmune disease.

Abstract: Two-domain MHC polypeptides are useful for modulating activities of antigen-specific T-cells, including for modulating pathogenic potential and effects of antigen-specific T-cells. Exemplary MHC class II-based recombinant T-cell ligands (RTLs) of the invention include covalently linked ?1 and ?1 domains, and MHC class I-based molecules that comprise covalently linked ?1 and ?2 domains. These polypeptides may also include covalently linked antigenic determinants, toxic moieties, and/or detectable labels. The disclosed polypeptides can be used to target antigen-specific T-cells, and are useful, among other things, to detect and purify antigen-specific T-cells, to induce or activate T-cells, to modulate T-cell activity, including by regulatory switching of T-cell cytokine and adhesion molecule expression, to treat conditions mediated by antigen-specific T-cells, including treatment and/or prevention of central nervous system damage relating to stroke.

Abstract: Methods and compositions are provided which confer protection against autoimmune diseases without triggering intracellular estrogen receptors. Such methods and compositions limit the side effects of steroids while providing the benefits conferred by such medications through the activation of membrane estrogen receptors.

Abstract: The invention provides a method of ameliorating a Th1-mediated immune pathology in a mammal. The method is practiced by administering a low dose of estrogen to the mammal. Optionally, an immunotherapeutic agent can also be administered to the mammal. Also provided are kits containing a low dose of estrogen and an immunotherapeutic agent.

Abstract: Two-domain MHC polypeptides are useful for modulating activities of antigen-specific T-cells, including for modulating pathogenic potential and effects of antigen-specific T-cells. Exemplary MHC class II-based recombinant T-cell ligands (RTLs) of the invention include covalently linked ?1 and ?1 domains, and MHC class I-based molecules that comprise covalently linked ?1 and ?2 domains. These polypeptides may also include covalently linked antigenic determinants, toxic moieties, and/or detectable labels. The disclosed polypeptides can be used to target antigen-specific T-cells, and are useful, among other things, to detect and purify antigen-specific T-cells, to induce or activate T-cells, to modulate T-cell activity, including by regulatory switching of T-cell cytokine and adhesion molecule expression, to treat conditions mediated by antigen-specific T-cells, to treat or prevent autoimmune or neurodegenerative diseases, to protect axons, and to prevent or reverse demyelination.

Abstract: The invention provides a method of ameliorating a Th1-mediated immune pathology in a mammal. The method is practiced by administering a low dose of estrogen to the mammal. Optionally, an immunotherapeutic agent can also be administered to the mammal. Also provided are kits containing a low dose of estrogen and an immunotherapeutic agent.

Abstract: The present disclosure relates to methods for inhibiting an autoimmune disease by administering to a subject a therapeutically effective amount of a composition that increases FOXP3 expression, thereby inhibiting the autoimmune disease. Further disclosed herein are methods for detecting in a subject an autoimmune disease or a predisposition to an autoimmune disease, and methods for assessing the efficacy of a therapy for an autoimmune disease.

Abstract: The invention provides a method of ameliorating a Th1-mediated immune pathology in a mammal. The method is practiced by administering a low dose of estrogen to the mammal. Optionally, an immunotherapeutic agent can also be administered to the mammal. Also provided are kits containing a low dose of estrogen and an immunotherapeutic agent.

Abstract: The invention provides a method of ameliorating a Th1-mediated immune pathology in a mammal. The method is practiced by administering a low dose of estrogen to the mammal. Optionally, an immunotherapeutic agent can also be administered to the mammal. Also provided are kits containing a low dose of estrogen and an immunotherapeutic agent.

Abstract: The invention provides a method of ameliorating a Th1-mediated immune pathology in a mammal. The method is practiced by administering a low dose of estrogen to the mammal. Optionally, an immunotherapeutic agent can also be administered to the mammal. Also provided are kits containing a low dose of estrogen and an immunotherapeutic agent.

Abstract: The invention provides a method of ameliorating a Th1-mediated immune pathology in a mammal. The method is practiced by administering a low dose of estrogen to the mammal. Optionally, an immunotherapeutic agent can also be administered to the mammal. Also provided are kits containing a low dose of estrogen and an immunotherapeutic agent.