Superantigen as a Promising Immunotherapy Treatment against Cancer: A Review Article

Abstract

Superantigens are toxins produced in hosts by some pathogenic microbes as a mechanism to sustain their pathogenicity. Superantigens are highly resistant to degradation by proteases enzyme, heat denaturation, and cause many dangerous diseases that in severe cases lead to death. Superantigens are atypical antigens that stimulate a profound proliferation of polyclonal T cells at low concentrations. All superantigens have a standard architecture even though they differ in amino acid sequences and are divided into two groups: endogenous superantigens and exogenous superantigens. The major histocompatibility complex molecules on antigen-presenting cells and T cell receptors on T cells are the major players in identifying foreign antigens. Superantigens can bind nonspecifically to both the major histocompatibility complex class II molecules and T cell receptors and form a trimolecular complex. Superantigens do not follow conventional antigens processing and presentation; they bind as intact macromolecules outside the antigen-binding groove of the major histocompatibility complex class II and to Vβ of T cells receptors. Thus, triggering an excessive release of proinflammatory cytokines, radiotherapy and chemotherapy often develop radio/drug resistance. Hence, cancer immunotherapy has been mainly considered as it instigates the patient’s immune system to fight cancer. Superantigens are one of the most potent T cell mitogens as 0.1 pg/ml is adequate to excite T lymphocytes. Accordingly, extensive in-vivo/in-vitro investigations have been conducted on the potential role of superantigens in eradicating tumors. The safety and effectiveness of superantigens as a cancer treatment have been verified in many clinical trials. Nevertheless, the vast inflammation after the potent T cell activation is known to promote diseases, including cancer. This paper reviews the potentiality of superantigen as an immunotherapy treatment against cancer.