AI Article Synopsis

  • Regulatory T (Treg) cells play a crucial role in preventing autoimmunity but also inhibit the immune system's ability to fight tumors, reducing cancer immunosurveillance.
  • Research found that depleting Treg cells via a specific target called GARP can promote stronger anti-tumor immune responses.
  • The novel monoclonal antibody DS-1055a effectively removes GARP+ Treg cells, activates effector T cells, and shows promising anti-tumor effects in mice with cancer, suggesting its potential as a new cancer immunotherapy.

Article Abstract

Regulatory T (Treg) cells, which are essential for maintaining self-tolerance, inhibit anti-tumor immunity, consequently hindering protective cancer immunosurveillance, and hampering effective anti-tumor immune responses in tumor-bearing hosts. Here, we show that depletion of Treg cells via targeting glycoprotein A repetitions predominant (GARP) induces effective anti-tumor immune responses. GARP was specifically expressed by highly suppressive Treg cells in the tumor microenvironment (TME) of multiple cancer types in humans. In the periphery, GARP was selectively induced in Treg cells, but not in effector T cells, by polyclonal stimulation. DS-1055a, a novel afucosylated anti-human GARP monoclonal antibody, efficiently depleted GARP+ Treg cells, leading to the activation of effector T cells. Moreover, DS-1055a decreased FoxP3+CD4+ T cells in the TME and exhibited remarkable anti-tumor activity in humanized mice bearing HT-29 tumors. We propose that DS-1055a is a new Treg-cell-targeted cancer immunotherapy agent with augmentation of anti-tumor immunity.

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http://dx.doi.org/10.1093/intimm/dxab027DOI Listing

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