The adaptive and innate immune systems are 2 parallel defensive networks, both of which are augmented by IRX-2.


The adaptive or acquired immune system is characterized by the ability of specialized cells to specifically recognize and attack pathogens and cancer using antigen-specific receptors found on the surfaces of immune cells.

Exposure of the immune system to antigens leads to the formation of immunological memory through the generation of long-lived, antigen-specific cells that results in an enhanced immune response upon repeat exposure to the same antigen.

The immune response consists of:

  • Humoral immunity: the production of antibodies that bind antigens in solution or on the surface of cells
  • Cell-mediated immunity: the generation of activated T cells capable of destroying pathogens and cancer cells bearing the target antigen on their surfaces

The adaptive immune system relies on the ability of certain cells, including B cells, macrophages, and dendritic cells to present antigen to T cells, a process that leads to T-cell activation.

The adaptive system is tightly regulated to avoid excessive or inappropriate immune responses. One such regulatory mechanism is the function of immune checkpoints, which down-regulate immune function. Numerous checkpoints have been identified, the best known of which is the PD-1:PD-L1 system. Checkpoint inhibition is an emerging mechanism of anticancer treatment.


The innate or nonspecific immune system is an evolutionarily older, parallel immune system that responds to pathogens and cancer cells in a generic way, rather than through recognition of specific antigenic molecules. The innate immune system includes certain types of white blood cells, notably macrophages and neutrophils, and the molecules of the complement cascade.

A component of the innate immune system that plays an important role in the defense against cancer is the natural killer (NK) cell, so named because it does not require activation to exert its cytotoxic effect. NK cells recognize cancer cells through altered expression of normal “self” cell surface antigens, which is common in malignancy.1

© 2017 IRX Therapeutics