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2001 APR 11 - (NewsRx.com & NewsRx.net) --
New discoveries about how individuals acquire long-term immunity against diseases are proving essential for the development of new vaccines for complex and persistent diseases such as HIV, malaria, and tuberculosis.
Rafi Ahmed, PhD, director of the Emory University Vaccine Center and a Georgia Research Alliance Eminent Scholar, discussed the links between mechanisms of long-term memory and vaccines in a lecture at the Experimental Biology 2001 Meeting on April 3, 2001. Ahmed was one of three immunologists selected to deliver the American Association of Immunologists Distinguished Lecture at this year's meeting.
In the past, scientists used a hit-or-miss approach to the development of vaccines for diseases like polio, yellow fever, or measles. Vaccine development for diseases such as HIV, however, which are expert immune-system evaders, require a detailed understanding of exactly how the immune response works.
Acute viral infections produce two types of long-term memory: humoral immunity, in which B cells produce antibodies to prevent infection by viruses, and cellular immunity, in which T cells activated by specific viral antigens kill the virus-infected cells and also produce cytokines, proteins that prevent the growth of viruses and make cells resistant to viral infection.
Ahmed and his colleagues previously found that plasma cells, the B cells that produce antibodies, live for quite a long time - sometimes for the entire life of an organism - which helps explain why humoral immunity is capable of such long-term persistence. The other aspect of immunity - the response of T cells to viruses - is much different than the B cell response, Ahmed explains.
CD4 T cells and CD8 T cells, which kill virus-infected cells, are of three types: naive cells, effector cells, or memory cells. Following exposure to virus or vaccination, T cells respond in a phase called "antigen-driven expansion," in which naive T cells are activated and undergo a dramatic 50,000- to 100,000-fold increase in number, resulting in an expanded population of cells. These effector cells kill virus-infected cells or produce cytokines. The effector-cell response lasts for only a few weeks, then the majority of effector cells die and about 5%-10% become memory cells. When memory cells come into contact with the original virus, they mount an immediate, strong, and rapid immune response.
Source: HighBeam Research, Scientists Provide New Details About Long-Term Immune Memory.(Brief...