Abstract: Provided herein are transplantation methods and methods of treating an inflammatory condition, ischemia reperfusion injury, infection, or a wound in a patient, comprising administering isolated IL-33 matrix-bound vesicles to the patient, as well as in vitro-expanded Treg cells. Also provided is a kit comprising IL-33 matrix-bound vesicles and in vitro-expanded Treg cells.

Abstract: Pre-existing alloreactive memory T cells are a major barrier to the induction of allograft tolerance in organ transplant recipients. The use of Eomesodermin (Eomes) expression in memory T cells to determine the risk of allograft rejection in a subject is described. Also described is the use of Eomes expression in memory T cells of transplant recipients to modify immunosuppressive therapy.

Abstract: Pre-existing alloreactive memory T cells are a major barrier to the induction of allograft tolerance in organ transplant recipients. The use of Eomesodermin (Eomes) expression in memory T cells to determine the risk of allograft rejection in a subject is described. Also described is the use of Eomes expression in memory T cells of transplant recipients to modify immunosuppressive therapy.

Abstract: The absence of regulatory T cells (Treg) may underlie disorders including but not limited to autoimmunity, dermatitis, periodontitis and even transplant rejection. Enhancing local numbers of Treg through in situ Treg expansion or induction is contemplated herein as a treatment option for these disorders. Current methods for in vivo Treg expansion are not Treg specific and are associated with many adverse side-effects. The data presented herein provides in vitro testing of a Treg-inducing microparticle providing a predictable controlled release for combinations of cytokines and drugs (e.g., IL-2, TGF-?, and/or rapamycin) resulting in targeted Treg migration. These controlled release microparticles are also capable of inducing FoxP3+ Treg in human cells in vitro suggesting that these compositions be developed into an in vivo Treg induction and expansion therapy.

Abstract: The absence of regulatory T cells (Treg) may underlie disorders including but not limited to autoimmunity, dermatitis, periodontitis and even transplant rejection. Enhancing local numbers of Treg through in situ Treg expansion or induction is contemplated herein as a treatment option for these disorders. Current methods for in vivo Treg expansion are not Treg specific and are associated with many adverse side-effects. The data presented herein provides in vitro testing of a Treg-inducing microparticle providing a predictable controlled release for combinations of cytokines and drugs (e.g., IL-2, TGF-?, and/or rapamycin) resulting in targeted Treg migration. These controlled release microparticles are also capable of inducing FoxP3+ Treg in human cells in vitro suggesting that these compositions be developed into an in vivo Treg induction and expansion therapy.

Abstract: Pre-existing alloreactive memory T cells are a major barrier to the induction of allograft tolerance in organ transplant recipients. The use of Eomesodermin (Eomes) expression in memory T cells to determine the risk of allograft rejection in a subject is described. Also described is the use of Eomes expression in memory T cells of transplant recipients to modify immunosuppressive therapy.

Abstract: The absence of regulatory T cells (Treg) may underlie disorders including but not limited to autoimmunity, dermatitis, periodontitis and even transplant rejection. Enhancing local numbers of Treg through in situ Treg expansion or induction is contemplated herein as a treatment option for these disorders. Current methods for in vivo Treg expansion are not Treg specific and are associated with many adverse side-effects. The data presented herein provides in vitro testing of a Treg-inducing microparticle providing a predictable controlled release for combinations of cytokines and drugs (e.g., IL-2, TGF-?, and/or rapamycin) resulting in targeted Treg migration. These controlled release microparticles are also capable of inducing FoxP3+ Treg in human cells in vitro suggesting that these compositions be developed into an in vivo Treg induction and expansion therapy.

Abstract: Provided is a method of identifying tolerance in allograft recipients. It has been found that higher levels of circulating plasmacytoid DC (pDC2 cells), as compared to monocytoid (pDC1) cells (pDC2/pDC1) correlates with transplant tolerance. In one embodiment, the method includes determining the relative amounts of HLA-DR+lin−(CD3−CD−14−CD19−CD20−)CD123+CD11c−(pDC2) cells and HLA-DR+lin−CD123loCD11c+(pDC1) cells in peripheral blood. The pDC1/pDC2 either can be determined from direct analysis of cells in a peripheral blood sample, or DC1 and DC2 cells can be cultured from a peripheral blood sample and the numbers of pDC1 and pDC2 cells in the peripheral blood sample can be estimated from the growth of the DC1 and DC2 cells in culture.

Abstract: A novel transplantation method for enhancing tolerogenicity in a host mammal to a transplant graft specimen from a donor mammal is disclosed. According to this method, immature mammalian dendritic cells propagated in the presence of a cytokine are administered to the host mammal in advance of transplantation. Tolerogenicity is enhanced in the host mammal when the immature mammalian dendritic cells concentrate in T-dependent regions of secondary lymphoid tissue of the host mammal, where the expression of major histocompatibility complex class II antigen by the immature mammalian dendritic cells is upregulated. Also disclosed is a novel method of effecting the maturation of immature dendritic cells in the presence of a cytokine and an extracellular matrix protein. These mature mammalian dendritic cells, which upregulate the expression of major histocompatibility complex class II antigen, can then be used to enhance the immune response of a host mammal.

Abstract: A novel transplantation method for enhancing tolerogenicity in a host mammal to a transplant graft specimen from a donor mammal is disclosed. According to this method, immature mammalian dendritic cells propagated in the presence of a cytokine are administered to the host mammal in advance of transplantation. Tolerogenicity is enhanced in the host mammal when the immature mammalian dendritic cells concentrate in T-dependent regions of secondary lymphoid tissue of the host mammal, where the expression of major histocompatibility complex class II antigen by the immature mammalian dendritic cells is upregulated. Also disclosed is a novel method of effecting the maturation of immature dendritic cells in the presence of a cytokine and an extracellular matrix protein. These mature mammalian dendritic cells, which upregulate the expression of major histocompatibility complex class II antigen, can then be used to enhance the immune response of a host mammal.