Antibody-mediated blockade of FCRL6

  • Some cancers protect themselves from attack by stimulating immune checkpoint targets.
  • Most tumors are heterogeneous and targeted therapy can leave surviving cancer cells to proliferate.
  • FCRL6 was identified as a checkpoint inhibitor, and when targeted with a specific antibody, the immune response is increased along with IFN-gamma and TNF-alpha production in CD8+ T cells.

Abstract

In recent years, there has been an increased understanding and exploitation of immune checkpoints in the T cell immune response. Normally, the immune system self-regulates to prevent an overreactive response from causing harm. However, this reduced immune response attenuates the potential therapeutic value of the immune system for defeating cancer. Thus, there has been an uptick in immune checkpoint therapies, which can increase the immune response regardless of the molecular signature of a tumor. This is particularly useful since it has been discovered that most tumors are heterogeneous, therefore, a targeted therapy, while effective for a while, can result in cancer re-emergence as cells not defeated by this type of therapy proliferate. This often results in the reemergence of cancer. Dr. Randall Davis at UAB has identified a potential target for immune checkpoint therapy.

Advantages

FCRL6 is a potential therapeutic target for cancer immunotherapy.

Potential Applications

This checkpoint inhibitor is relatively unexplored, and could offer a competitive advantage as an effective target to increase the immune response to some cancers, mainly after progression from anti-PD1 therapy.

Contact Information

Name: Diptiman Chanda

Email: dip6nov@uab.edu

Phone: (205) 934-7871