Some tumors and certain viral infections pose a challenge to the human body which the immune system cells; typically fails to hand. In these diseases it switches to hypofunctional state that prevent adequate protection; by identifying the crucial molecular switch that triggers such dysfunctional immunity responses.
Dysfunctional immune responses this could make it possible in the future to switch off or to prevent this state; Cytotoxic T-cells are essential mediators of protective immunity to viral infection and malignant tumors and are a key target for immunotherapy approaches; prolonging exposure to cognate antigen often attenuates the effector capacity of T-cells and limits their therapeutic potential.
Exhaustion mode of immune cells
Normally, the immunuty system goes into a state of maximum alert following a viral infection; It triggering the activation of a variety of immune cells such as T and B cells. These procreate in large numbers; and aggressively combat the infected cells; The deactivation of immunity responses may also permit massive growth of tumors.
The protein Tox is the decisive molecular switch; by using the mouse and cell culture models together with the patient samples; the scientists fing out that the protein has an effect inside the cell nucleus; the cell where it activates a genetic program that alters the immune cell function; But as a result; the inhibitory surface receptors appear on the surface of the immune cells.
Excessive immune response
But this is the absolute prerequisite for targeted modification of the processes. Controlling Tox could make it possible to reactivate weak immune responses; which would be interesting for example in fighting tumors,; or to slow excessive immune responses like those found in autoimmune diseases
The cells are thus open to inhibitory signals; ensuring that the cells tire; functioning less effectively or even dying off; Tox as a critical factor for the normal progression of T cell dysfunction; for the maintenance of exhausted T cells during chronic infection; and we document a link between CD8 T cell intrinsic suppression of effector function and protection against pathology.