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18.0 Abstract: Tumor Immunology and Immunotherapy Program The overarching goal of the Tumor Immunology and Immunotherapy (TII) Program of UMGCC is to develop and implement immune-based strategies to prevent, treat, and/or monitor malignant diseases and disease progression. To achieve this goal, the program focuses on three specific aims: Theme 1: Cell-based cancer immunotherapies—elicit active tumor immunity capable of reducing or preventing malignant cell growth; Theme 2: Inhibiting immunosuppression—develop strategies to overcome tumor immune evasion; and Theme 3: Cancer and inflammation—elucidate the roles for infection and inflammatory responses in cancer development. The successful implementation of this work is facilitated by strong interactions between clinicians and basic researchers. Program research and mentoring strategies are designed to promote inter- and intraprogrammatic interaction and mentoring of junior research and clinical faculty. The TII program has 60 members representing 17 academic departments and 5 schools/colleges of the University of Maryland. Members of the program conduct cancer-focused research that receives $4.1 million total annual funding, including $0.6 million from NCI and $2.6 million from other peer-reviewed sources. In addition, TII Program members receive $0.9 million annually from non-peer-reviewed funding sources. Between January 2010 and December 2014, TII members authored 366 cancer-related publications, of which 21 percent resulted from intraprogrammatic and 22 percent from interprogrammatic collaborations. Approximately 52 percent of the publications represent collaborations with external investigators. Research efforts by TII faculty are supported by extensive use of the FCSS, BSS, and PBSS.
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Beta-2 adrenergic signaling in immune homeostasis and reconstitution
CD27/CD70 mediated negative regulation of inflammatory T cell responses
  • 批准号:
    10226021
  • 项目类别:
  • 资助金额:
    $58.61万
  • 财政年份:
    2018
  • 负责人:
    Xuefang Cao
  • 依托单位:
CD27/CD70 mediated negative regulation of inflammatory T cell responses
Targeting Granzyme B to Separate GVH from GVL Responses
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