T cells and antibody-producing B cells carry out immune defense against specific pathogens such as viruses. Antibodies and T cell receptors are highly diverse molecules that can recognize millions of different molecules. Upon encounter of a foreign antigen (such as a molecule from the surface of a virus), T cells and B cells whose receptors match that particular antigen expand dramatically, providing the immune system with a large number of very specific defenders. After an attack is fought off, the overall numbers of specific T and B cells go down again, but a few of them become long-lived so-called "memory cells" that ensure a quick re-mobilization should the same type of attacker strike again.
T cells consist of two major groups: CD4-positive T helper cells (who help other immune cells in mounting an effective response) and CD8-positive killer T cells. HIV infects and destroys CD4-positive cells, leaving patients with a crippled immune system. Throughout the course of HIV disease, however, patients have high levels of HIV-specific killer T cells. Early after initial infection, these cells are able to effectively kill the virus and reduce viral load. On the other hand, during the later stage of disease killer T cells, while still present, seem no longer able to control the virus. In an article in the November 4 issue of the Journal of Clinical Investigation, Premlata Shankar and colleagues from the Center for Blood Research at Harvard Medical School suggest why this might be the case.
The researchers compared killer T cells from HIV infected asymptomic individuals with those from symptomatic AIDS patients. They examined the killer cells ability to eliminate target cells infected with laboratory strains of HIV on one hand, and with autologous virus (isolated from the patient) on the other. What they found is that killer T cells from asymptomatic individuals can recognize and kill both types of target cells. In contrast, the killer T cells from symptomatic patients, while still able to recognize and eliminate the laboratory strain targets, no longer killed target cells that were infected with their own, autologous, virus. This is likely due to the virus propensity to mutate and the in inability of the patients weakened immune system to keep up with the changing virus.
Brooke Grindlinger | EurekAlert!
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