Abstract
TCR Vβ usage was examined in C57BL/6 mice infected with Plasmodium yoelii. In addition to a polyclonal T cell activation, already described, a superantigenic-like activity was observed during the acute infection. This superantigenic activity induces a preferential deletion without prior expansion of CD4+ and CD8+ T cells bearing the TCR Vβ9 segment. The superantigen could be released by the parasite at different stages of its development since the deletion of Vβ9+ T cells was observed in blood and lymph nodes of mice infected either with sporozoites or with erythrocytic stages. Injection of sporozoite or parasitized erythrocytes to newborn mice led to a deletion and anergy of peripheral Vβ9+ T cells, without affecting thymic T cell populations. These observations suggest that the superantigen is released at very low concentrations during parasite development. The role of such parasite superantigenic activity in infectivity can be underlined by the observation that congenic BALB.D2 Mls1a mice lacking V(β)9 T cells are more susceptible to infection by P. yoelii.
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CITATION STYLE
Pied, S., Voegtle, D., Marussig, M., Rénia, L., Miltgen, F., Mazier, D., & Cazenave, P. A. (1997). Evidence for superantigenic activity during murine malaria infection. International Immunology, 9(1), 17–25. https://doi.org/10.1093/intimm/9.1.17
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