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Theme 1: Innate immunity and signaling mechanisms

Overview  

One reason many current forms of cancer immunotherapy have low clinical response rates is because they fail to activate the innate immune system - a prerequisite for forming long-lasting adaptive immune responses that are necessary to eliminate tumors and prevent their recurrence.  

Several CCIR members are investigating the development and function of innate immune cells and receptor-mediated signal transduction pathways leading to expression of cytokines and costimulatory molecules involved in T cell activation and differentiation in order to find ways to enable cancer immunotherapy to activate innate immunity leading to durable anti-tumor T cell responses.  

Some highlights from Fiscal Year 2013 include:  

  • A recent study used unbiased approaches to demonstrate that vimentin is a shared autoantigen recognized by nonstereotyped follicular lymphoma BCRs and also recognized by the Igs of mantle cell lymphoma and multiple myeloma, suggesting that vimentin may play a role in the pathogenesis of multiple B cell malignancies (Cha SC, J Immunol. 2013)
  • Findings from a study published in Nature established OTUD7B, a novel deubiquitinase, as a crucial regulator of signal-induced non-canonical NF-κB activation, allowing the authors to propose a mechanism of immune regulation that involves OTUD7B-mediated deubiquitination and stabilization of TRAF3 (Hu H, Nature, 2013)
  • CD13+ bone marrow-derived myeloid cells promote angiogenesis, tumor growth, and metastasis (Dondossola E, PNAS. 2013)

Additional Relevant Publications


© 2014 The University of Texas MD Anderson Cancer Center