Infection Possibly Reverses Host Immunosuppression to Restrain Tumor Growth

Tumor cells can successfully escape the host immune attack by inducing the production of immunosuppressive cells and molecules, leading to an ineffective tumor treatment and poor prognosis. Although immunotherapies have improved the survival rate of cancer patients in recent years, more effective drugs and therapies still need to be developed. As an intracellular parasite, can trigger a strong Th1 immune response in host cells, including upregulating the expression of interleukin-12 (IL-12) and interferon-γ (IFN-γ). Non-replicating uracil auxotrophic strains of were used to safely reverse the immunosuppression manipulated by the tumor microenvironment. In addition to the whole lysate antigens, -secreted effectors, including profilin, rhoptry proteins (ROPs), and dense granule antigens (GRAs), are involved in arousing the host's antigen presentation system to suppress tumors. When infection relieves immunosuppression, tumor-related myeloid cells, including macrophages and dendritic cells (DCs), are transformed into immunostimulatory phenotypes, showing a powerful Th1 immune response mediated by CD8 T cells. Afterwards, they target and kill the tumor cells, and ultimately reduce the size and weight of tumor tissues. This article reviews the latest applications of in tumor therapy, including the activation of cellular immunity and the related signal pathways, which will help us understand why infection can restrain tumor growth.