T suppressor cell

CD8+ T suppressor cells predominate in patients with no protective immunity (visceral leishmaniasis patients).

Once this happens, anti-HIV antibodies can bind to and kill most of the host's T suppressor cell population.

Hence in this model, the onset of AIDS is primarily an auto-immune reaction triggered by the cross-reaction of anti-HIV antibodies with T suppressor cells.

Benezra has theorized that a large amount of CD8+ T suppressor cells are observed in the later stages of the disease in order to down regulate the inflammatory immune reaction.

These findings suggest that antigen stimulation of CD4+ helper T cells results in production of cytokines that kill or down regulate CD8+ T suppressor cells.

Once the leishmania infection has been eliminated and leishmania antigens are gone, CD8+ T suppressor cells down-regulate CD4+ T helper cells.

These three quasispecies apply selective pressure on one another and co-evolve in such a way that the viral epitopes eventually come to mimick the V regions of the main population of T suppressor cells.

Isolation of cytokines that inhibit and kill CD8+ T suppressor cells might be useful in treating diseases that involve immune suppression such as leishmaniasis, AIDS, and certain cancers.

Following an infection with HIV that manages to establish itself, there is a complex interaction between the HIV virus, the T helper cells that it infects, and T suppressor cells.