[1] The phenomenon was originally referred to as "reverse chemotaxis," and later, “fugetaxis” (derived from the Latin words fugere, to flee from; and taxis, movement).
During the development of the Central Nervous System, chemokinetic agents influence the localization of neuronal cells by either attracting or repelling the growing axon.
[6] Immune privilege is thought to be an evolutionary adaptation to protect the most vital sensory organs and reproductive structures that would be otherwise severely impaired during an inflammatory response.
These characteristics include: T-cells are one of the most critical constituents of the adaptive immune system due to their ability to continue developing after activation.
[8] To prevent premature instigation, it is necessary for T-cells to mature in an environment completely isolated from any potentially activating factors (antigens, cytokines, steroids, receptor antagonists, adhesion molecules, etc.).
[9] As a result, T-cells are formed in the bone marrow and subsequently migrate to the cortex of the thymus where they can mature in an antigen-free environment.
For example, T-helper, T-cytotoxic, T-memory, and T-suppressor cells all develop in the thymus and must leave it to provide their functions elsewhere in the body during an immune response.
[10] In vitro models of the T-lymphopoiesis system have revealed that the emigration of mature T-cells occurs as a result of immunorepulsion away from a chemokinetic agent generated from within the thymic organ via a G-protein coupled receptor.
[20] One study showed that high expression of SDF-1 was responsible for the down-regulation of MHC class I molecules, which significantly interferes with tumor antigen recognition.
These chemical factors induce all associated inflammatory symptoms by sensitizing pain receptors, causing vasodilation of the blood vessels at the scene, and attracting phagocytes.
The cells attack pathogens by releasing strong oxidizing agents including hydrogen peroxide, free oxygen radicals, and hypochlorite.
If attainable, constitutive expression of chemorepellents by the donor tissue would create an inducible immune-privileged site for the allograft, and would be an effective alternative treatment for graft rejection prevention.
The gradient signal of the chemokinetic agent is received through specific receptors on the cell surface and is transduced through intracellular machinery to generate the directional response.
In addition to axon growth cones, the model organism Dictyostelium discoideum has been instrumental in determining the mechanisms that mediate chemorepulsion and immunorepulsion.