The functional role of γδ T cells (expressing the γδ heterodimeric T- cell receptor for antigen) in infectious diseases remains largely unknown. We have therefore attempted to define the possible role of these T cells in the immune response against the various developmental stages of malaria parasites. For this purpose, we monitored the immune response and the development of liver and blood stages of Plasmodium yoelii, a rodent malaria parasite, in immunized and nonimmunized αβ T-cell-deficient and γδ T- cell-deficient mice. Immunization of αβ T-cell-deficient mice with irradiated sporozoites induced an immune response that significantly inhibited the development of the parasite's liver stages. This inhibitory immune response was abolished by an antibody-mediated transient in vivo depletion of γδ T cells. Two γδ T-cell clones were derived from malaria- immunized αβ T-cell-deficient mice. The adoptive transfer of one of these γδ T-cell clones to normal mice inhibited the development of liver stages, following sporozoite inoculation. These results provide evidence for γδ T- cell-mediated protective immunity against parasites, in the absence of αβ T cells. As for the blood phase of the infection, both normal mice and γδ T- cell-deficient mice cleared the blood stages of the nonlethal strain of P. yoelii, while αβ T-cell-deficient mice failed to control the parasitemia.
|Original language||English (US)|
|Number of pages||5|
|Journal||Proceedings of the National Academy of Sciences of the United States of America|
|Publication status||Published - Jan 4 1994|
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