AIDSWEEKLY Plus; Monday, December 28, 1998
Daniel J. DeNoon, Senior Editor
Such immunity is critical for prevention of diseases such as tuberculosis, leishmaniasis, and AIDS.
NIH researchers Sanjay Gurunathan, Robert A. Seder, and colleagues conducted mouse experiments showing that cellular immunity elicited by vaccination lasts far longer when there is persistent production of the cytokine interleukin-12 (IL-12).
"The persistence of IL-12 may be the essential determinant in maintaining durable cell-mediated immune responses for an intracellular parasitic infection," Gurunathan et al. wrote in the journal Nature Medicine ("Vaccine Requirements for Sustained Cellular Immunity To An Intracellular Parasitic Infection," Nature Med, 1998;4(12):1409-15).
Nearly all vaccines currently in use work by stimulating antibody- mediated immunity, which is supported by T-helper type 2 (Th2) cytokines. However, intracellular pathogens such as Leishmania major, Mycobacterium tuberculosis, and HIV can be controlled only by cell- mediated immunity, which is supported by Th1 cytokines. Unfortunately, science currently lacks an understanding of how to maintain this latter class of responses.
Using the mouse model of L. major, Gurunathan et al. explored the use of the Th1 cytokine IL-12 as a vaccine adjuvant. Their first set of experiments showed that vaccination with plasmid DNA encoding a specific L. major antigen elicited longer-lasting immunity than leishmanial protein plus recombinant IL-12 (rIL-12). A second set of experiments showed that cellular immunity elicited by vaccination with leishmanial protein plus IL-12 DNA lasted far longer than that elicited by leishmanial protein plus IL-12 protein.
"These data demonstrate the importance [of] the persistence of IL- 12 in maintaining long-term cellular immunity and provide a rationale for designing vaccines for intracellular infections requiring these types of responses," Gurunathan et al. wrote.
The authors suggested that IL-12 protein may be very useful as an adjuvant for the attenuated bacillus Calmette-Guerin (BCG) tuberculosis vaccine.
"One mechanism that could 'restore' the magnitude of the Th1 response is to combine IL-12 protein with BCG at the time of vaccination," they wrote. "Then, as BCG is a live vaccine, it could provide a continuous source of both antigen and IL-12 able to perpetuate this enhanced response."
Preliminary murine studies supported this hypothesis.
The corresponding author for this study is Robert A. Seder, National Institutes of Health, Bethesda, Maryland 20892. Email: <rseder@nih.gov>.
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