Title:CTLA-4: As an Immunosuppressive Immune Checkpoint in Breast
Cancer
Volume: 23
Issue: 6
Author(s): Shaho Ghahremani Dehbokri, Nazila Alizadeh, Alireza Isazadeh, Amir Baghbanzadeh, Soheil Abbaspour-Ravasjani, Khalil Hajiasgharzadeh and Behzad Baradaran*
Affiliation:
- Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
Keywords:
Breast cancer, CTLA-4, immunotherapy, monoclonal antibody, immune, immunosuppressive, immune checkpoint.
Abstract: Breast cancer (BC) is one of the prevalent diseases and causes of death in
women, and its incidence rate is increasing in numerous developed and developing
countries. The common approach to BC therapy is surgery, followed by radiation therapy
or chemotherapy, which doesn't lead to acceptable outcomes in many patients.
Therefore, developing innovative strategies for treating BC is essential for the most
effective therapy. The immunotherapy of BC is a promising and attractive strategy that
can increase the immune system's capacity to recognize and kill the tumor cells, inhibit
the recurrence of the tumors, and develop new metastatic sites. The blockade of
immune checkpoints is the most attractive and promising strategy for cancer
immunotherapy. The cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) is a cellsurface
glycoprotein expressed by stimulated T cells and has pivotal roles in cell cycle
modulation, cytokine generation, and regulation of T cell proliferation. Currently, anti-
CTLA-4 agents such as monoclonal antibodies (Ipilimumab and tremelimumab) are
broadly applied as therapeutic agents in clinical studies of different cancers. The anti-
CTLA-4 antibodies, alone or combined with other therapeutic agents, remarkably
increased the tumor-suppressive effects of the immune system and improved the
prognosis of cancer. The immune checkpoint inhibitors may represent promising options
for BC treatment as in monotherapy or in combination with other conventional
treatments. In this review, we discuss the role of CTLA-4 and its therapeutic potential by
inhibitors of immune checkpoints in BC therapeutics.
