Abstract: Provided are exosomes derived from V?2-T cell (V?2-T-Exos) for killing or inhibiting EBV-infected cells. Further provided is a method for killing or inhibiting the growth of an EBV-infected cell, comprising contacting the EBV-infected cell with exosomes from V?2+ T cells in an amount effective to kill or inhibit the growth of the cell. Preferably, the EBV-infected cell is an EBV-infected cell that has become neoplastic, such as an EBV-infected neoplastic B-cell or an EBV-infected neoplastic epithelial cell. Further provided is a method for treating an EBV-induced cancer in a subject by administering to the subject a therapeutically effective amount of V?2-T-Exos. V?2-T-Exos can be derived from V?2-T cells obtained from the subject or from an allogeneic healthy individual. Methods for isolating V?2-T-Exos from V?2-T cells are also provided.

Abstract: Graft-versus-host disease (GVHD) is a lethal complication of allograft transplantation. The current strategy of using immunosuppressive agents to control GVHD may cause general immune suppression and limit the effectiveness of allograft transplantation. Adoptive transfer of regulatory T cells (Treg) can prevent GVHD in rodents, indicating the therapeutic potential of Treg for GVHD in humans. However, the clinical application of Treg-based therapy is hampered by the low frequency of human Treg and the lack of a reliable model to test their therapeutic effects in vivo. Human alloantigen-specific Treg are generated from antigenically-naïve precursors in a large scale ex vivo using allogeneic activated B cells as stimulators. Here, a human allogeneic GVHD model is established in humanized mice to mimic GVHD after allograft transplantation in humans.

Abstract: Aminobisphosphonate pamidronate (PAM) can control Epstein-Barr virus (EBV) associated disorders in humanized mice through a V?9V?2-T-cell dependent mechanism. This suggests a strong potential for a therapeutic approach using PAM to boost human V?9V?2-T-cell immunity against EBV associated disorders, such as the lymphoproliferative disease (LPD), posttransplant lymphoproliferative disorder (PLPD), Hodgkin's disease, Burkitt's lymphoma, and nasopharyngeal carcinoma (NPC).

Abstract: Graft-versus-host disease (GVHD) is a lethal complication of allograft transplantation. The current strategy of using immunosuppressive agents to control GVHD may cause general immune suppression and limit the effectiveness of allograft transplantation. Adoptive transfer of regulatory T cells (Treg) can prevent GVHD in rodents, indicating the therapeutic potential of Treg for GVHD in humans. However, the clinical application of Treg-based therapy is hampered by the low frequency of human Treg and the lack of a reliable model to test their therapeutic effects in vivo. Human alloantigen-specific Treg are generated from antigenically-naïve precursors in a large scale ex vivo using allogeneic activated B cells as stimulators. Here, a human allogeneic GVHD model is established in humanized mice to mimic GVHD after allograft transplantation in humans.

Abstract: Graft-versus-host disease (GVHD) is a lethal complication of allograft transplantation. The current strategy of using immunosuppressive agents to control GVHD may cause general immune suppression and limit the effectiveness of allograft transplantation. Adoptive transfer of regulatory T cells (Treg) can prevent GVHD in rodents, indicating the therapeutic potential of Treg for GVHD in humans. However, the clinical application of Treg-based therapy is hampered by the low frequency of human Treg and the lack of a reliable model to test their therapeutic effects in vivo. Human alloantigen-specific Treg are generated from antigenically-naïve precursors in a large scale ex vivo using allogeneic activated B cells as stimulators. Here, a human allogeneic GVHD model is established in humanized mice to mimic GVHD after allograft transplantation in humans.

Abstract: Methods for inducing, expanding, and/or generating alloantigen-specific regulatory T cells. Alloantigen-specific regulatory T cells can be induced, expanded, and/or generated from naive CD4+CD25? T cells by using CD40-activated B cells. The regulatory T cells can be human T cells. In one embodiment, the alloantigen-specific human regulatory T cells can be CD4highCD25+Foxp3+ regulatory T cells.

Abstract: Aminobisphosphonate pamidronate (PAM) can control Epstein-Barr virus (EBV) associated disorders in humanized mice through a V?9V?2-T-cell dependent mechanism. This suggests a strong potential for a therapeutic approach using PAM to boost human V?9V?2-T-cell immunity against EBV associated disorders, such as the lymphoproliferative disease (LPD), posttransplant lymphoproliferative disorder (PLPD), Hodgkin's disease, Burkitt's lymphoma, and nasopharyngeal carcinoma (NPC).

Abstract: Graft-versus-host disease (GVHD) is a lethal complication of allograft transplantation. The current strategy of using immunosuppressive agents to control GVHD may cause general immune suppression and limit the effectiveness of allograft transplantation. Adoptive transfer of regulatory T cells (Treg) can prevent GVHD in rodents, indicating the therapeutic potential of Treg for GVHD in humans. However, the clinical application of Treg-based therapy is hampered by the low frequency of human Treg and the lack of a reliable model to test their therapeutic effects in vivo. Human alloantigen-specific Treg are generated from antigenically-naïve precursors in a large scale ex vivo using allogeneic activated B cells as stimulators. Here, a human allogeneic GVHD model is established in humanized mice to mimic GVHD after allograft transplantation in humans.

Abstract: Methods for inducing, expanding, and/or generating alloantigen-specific regulatory T cells. Alloantigen-specific regulatory T cells can be induced, expanded, and/or generated from naive CD4+CD25? T cells by using CD40-activated B cells. The regulatory T cells can be human T cells. In one embodiment, the alloantigen-specific human regulatory T cells can be CD4highCD25+Foxp3+ regulatory T cells.

Abstract: Methods for inducing, expanding, and/or generating alloantigen-specific regulatory T cells. Alloantigen-specific regulatory T cells can be induced, expanded, and/or generated from naive CD4+CD25? T cells by using CD40-activated B cells. The regulatory T cells can be human T cells. In one embodiment, the alloantigen-specific human regulatory T cells can be CD4highCD25+Foxp3+ regulatory T cells.

Abstract: Methods for inducing, expanding, and/or generating alloantigen-specific regulatory T cells. Alloantigen-specific regulatory T cells can be induced, expanded, and/or generated from naive CD4+CD25?T cells by using CD40? activated B cells. The regulatory T cells can be human T cells. In one embodiment, the alloantigen-specific human regulatory T cells can be CD4hIghCD25+Foxp3+ regulatory T cells.