Abstract: The present invention provides materials and methods related to culturing stable Treg cells or in vivo expansion of stable Treg cells, the cells made by the methods, treatments for various inflammatory/autoimmune pathologies and transplant/graft rejection, and related materials. Ex vivo induction and expansion of the stable Tregs is described, including use of inducing compositions, such as certain mAbs and other compounds, along with expansion medium comprising IL-2. In vivo expansion of stable Treg cells and treatments for various inflammatory/autoimmune pathologies and transplant/graft rejection are described, including the use of mAbs and their variants.

Abstract: The present invention provides materials and methods related to culturing stable Treg cells or in vivo expansion of stable Treg cells, the cells made by the methods, treatments for various inflammatory/autoimmune pathologies and transplant/graft rejection, and related materials. Ex vivo induction and expansion of the stable Tregs is described, including use of inducing compositions, such as certain mAbs and other compounds, along with expansion medium comprising IL-2. In vivo expansion of stable Treg cells and treatments for various inflammatory/autoimmune pathologies and transplant/graft rejection are described, including the use of mAbs and their variants.

Abstract: Methods are disclosed for inhibiting or disrupting Janus tyrosine kinase 3 (Jak3) dependent function in cells of lymphoid or myeloid origin, especially for blocking proliferation and function of lymphocytes (e.g., T-cells, B-cells). A Mannich base compound, or a derivative or modified compound, is employed which is capable of selectively inhibiting Jak3 while affecting other protein tyrosine kinase activities to a lesser extent or not at all, to provide beneficial effects such as mitigation of transplant rejection and alleviation of allergic responses with fewer side effects than with conventional immunosuppressive agents.

Abstract: An ex vivo method of expanding a population of regulatory T-cells includes culturing a starting population of cells containing CD4+CD25? T-cells in a growth medium; introducing nitric oxide into the growth medium sufficient to potentiate switching of the CD4+CD25? T-cells to CD4+CD25+ regulatory T-cells (Treg cells), whereby a subpopulation of Treg cells is produced; and allowing the Treg cells to proliferate in culture, to provide a final population of T-cells containing more Treg cells than were present in the original T-cells. The resulting expanded population of Treg cells are used to deter or decrease an undesired T-cell mediated immune response, e.g., allograft rejection, in a mammalian host by transplanting the Treg cells at a site of a potential or existing undesired immune response, whereby the undesired immune response is deterred or decreased.

Abstract: Methods are disclosed for inhibiting or disrupting Janus tyrosine kinase 3 (Jak3) dependent function in cells of lymphoid or myeloid origin, especially for blocking proliferation and function of lymphocytes (e.g., T-cells, B-cells). A Mannich base compound, or a derivative or modified compound, is employed which is capable of selectively inhibiting Jak3 while affecting other protein tyrosine kinase activities to a lesser extent or not at all, to provide beneficial effects such as mitigation of transplant rejection and alleviation of allergic responses with fewer side effects than with conventional immunosuppressive agents.

Abstract: Methods are disclosed for inhibiting or disrupting Janus tyrosine kinase 3 (Jak3) dependent function in cells of lymphoid or myeloid origin, especially for blocking proliferation and function of lymphocytes (e.g., T-cells, B-cells). A Mannich base compound, or a derivative or modified compound, is employed which is capable of selectively inhibiting Jak3 while affecting other protein tyrosine kinase activities to a lesser extent or not at all, to provide beneficial effects such as mitigation of transplant rejection and alleviation of allergic responses with fewer side effects than with conventional immunosuppressive agents.

Abstract: Chimeric MHC Class I molecules having a recipient-type N-terminus, a donor-type alpha-1 helical region, and a recipient-type alpha-2 domain induce tolerance to donor grafts when administered to the recipient at time of transplantation.

Abstract: Compositions and methods are provided for the prevention and treatment of allograft rejection. Compositions are provided which comprise an antisense oligonucleotide targeted to a nucleic acid sequence encoding intercellular adhesion molecule-1, vascular cell adhesion molecule-1, or endothelial leukocyte adhesion molecule-1 in combination with an immunosuppressive agent. Methods of preventing or treating allograft rejection by treating an allograft recipient with such a composition are provided. Methods for preventing allograft rejection comprising perfusion of the graft are also provided.