REVERSAL OF THE SUPPRESSIVE FUNCTION OF SPECIFIC T CELLS VIA TOLL-LIKE RECEPTOR 8 SIGNALING
    5.
    发明申请
    REVERSAL OF THE SUPPRESSIVE FUNCTION OF SPECIFIC T CELLS VIA TOLL-LIKE RECEPTOR 8 SIGNALING 审中-公开
    特异性T细胞通过类似受体8信号的抑制功能的反转

    公开(公告)号:US20080026986A1

    公开(公告)日:2008-01-31

    申请号:US11757235

    申请日:2007-06-01

    摘要: CD8+ regulatory T (Treg) cells and γδ Treg cells profoundly suppress host immune responses and thus protect against autoimmune disease while restricting desired immune responses such as antitumor immunity. Synthetic phosphorothioate-protected, guanosine-containing oligonucleotides can directly reverse the suppressive activity of Treg cells without involving dendritic cells. This effect appears to be transduced by signaling through Toll-like receptor (TLR) 8 and engagement of the MyD88 and IRAK4 molecules in Treg cells, in specific embodiments. Stimulation of Treg cells with natural ligands for human TLR8 recapitulated the effect of the synthetic guanosine-containing oligonucleotides.

    摘要翻译: CD8 + Treg细胞和Gammadelta Treg细胞深刻地抑制宿主免疫应答,从而防止自身免疫疾病,同时限制所需的免疫应答如抗肿瘤免疫。 合成的硫代磷酸酯保护的含鸟苷酸寡核苷酸可以直接逆转Treg细胞的抑制活性而不涉及树突状细胞。 在特定的实施方案中,这种作用似乎通过Toll样受体(TLR)8的信号转导和MyD88和IRAK4分子在Treg细胞中的接合而转导。 人TLR8天然配体对Treg细胞的刺​​激重现了含有合成含鸟苷酸的寡核苷酸的作用。

    Direct Reversal Of The Suppressive Function Of CD4+Regulatory T Cells Via Toll-Like Receptor 8 Signaling
    8.
    发明申请
    Direct Reversal Of The Suppressive Function Of CD4+Regulatory T Cells Via Toll-Like Receptor 8 Signaling 审中-公开
    通过Toll样受体8信号直接逆转CD4 +调节性T细胞的抑制功能

    公开(公告)号:US20090209620A1

    公开(公告)日:2009-08-20

    申请号:US11816902

    申请日:2006-03-09

    摘要: CD4+ regulatory T (Treg) cells profoundly suppress host immune responses and thus protect against autoimmune disease while restricting desired immune responses such as antitumor immunity. Synthetic phosphorothioate-protected, guanosine-containing oligonucleotides can directly reverse the suppressive activity of Treg cells without involving dendritic cells. This effect appears to be transduced by signaling through Toll-like receptor (TLR) 8 and engagement of the MyD88 and IRAK4 molecules in Treg cells. Stimulation of Treg cells with natural ligands for human TLR8 recapitulated the effect of the synthetic guanosine-containing oligonucleotides .

    摘要翻译: CD4 +调节T(Treg)细胞深刻地抑制宿主免疫应答,从而防止自身免疫疾病,同时限制所需的免疫应答如抗肿瘤免疫。 合成的硫代磷酸酯保护的含鸟苷酸寡核苷酸可以直接逆转Treg细胞的抑制活性而不涉及树突状细胞。 该效应似乎通过Toll样受体(TLR)8的信号转导和MyD88和IRAK4分子在Treg细胞中的结合来转导。 人TLR8天然配体对Treg细胞的刺​​激重现了含有合成含鸟苷酸的寡核苷酸的作用。

    Cancer peptides of NY-ESO-1/CAG-3
    9.
    发明授权
    Cancer peptides of NY-ESO-1/CAG-3 失效
    NY-ESO-1 / CAG-3的癌症肽

    公开(公告)号:US07084239B1

    公开(公告)日:2006-08-01

    申请号:US09529206

    申请日:1998-09-21

    CPC分类号: C07K14/4748 A61K38/00

    摘要: The present invention discloses the identification, isolation and cloning of a gene encoding a novel cancer antigen NY ESO-1CAG-3 and peptides thereof derived from various open reading frames from the NY ESO-1 gene. The novel cancer antigen and peptides are recognized by cytotoxic T lymphocytes in an HLA restricted manner. The products of the gene are promising candidates for immunotherapeutic strategies for the prevention, treatment and diagnosis of patients with cancer.

    摘要翻译: 本发明公开了从NY ESO-1基因衍生自各种开放阅读框的编码新型癌抗原NY ESO-1CAG-3的基因及其肽的鉴定,分离和克隆。 新型癌抗原和肽以HLA限制的方式被细胞毒性T淋巴细胞识别。 该基因的产物是用于预防,治疗和诊断癌症患者的免疫治疗策略的有希望的候选者。

    Identification of TRP-2 as a human tumor antigen recognized by cytotoxic T lymphocytes

    公开(公告)号:US07001600B1

    公开(公告)日:2006-02-21

    申请号:US09651210

    申请日:2000-08-30

    IPC分类号: A61K39/00

    CPC分类号: A61K39/0011 C07K14/4748

    摘要: The infusion of TIL586 along with interleukin-2 (IL-2) into the autologous patient with metastatic melanoma resulted in the objective regression of tumor. A gene encoding a tumor antigen recognized by TIL586 was previously isolated and shown to encode gp75 or TRP-1. The present invention relates to the identification of a second tumor antigen recognized by a HLA-A31 restricted CTL clone derived from the TIL586 cell line. This antigen derived from the TRP-2 protein tumor antigen and peptides thereof are capable of sensitizing target cells for lysis by a CTL clone at 1 nM peptide concentration. Modified peptides were also recognized by the CTL clone.