International Immunology, Vol. 11, No. 9, 1553-1562,
September 1999
© 1999 Japanese Society for Immunology
T cell response in malaria pathogenesis: selective increase in T cells carrying the TCR Vß8 during experimental cerebral malaria
1 INSERM U511, Immunobiologie Cellulaire et Moléculaire des Infections Parasitaires,CHU Pitié-Salpêtrière, 75643 Paris Cedex 13, France
2 CNRS URA 1961, Unité d'Immunochimie Analytique, Département d'Immunologie, Institut Pasteur,75724 Paris Cedex 15, France
Correspondence to: S. Pied, INSERM U511, CHU Pitié-Salpêtrière, 91 Boulevard de l'Hôpital, 75643 Paris Cedex 13, France
To characterize the T cells involved in the pathogenesis of cerebral malaria (CM) induced by infection with Plasmodium berghei ANKA clone 1.49L (PbA 1.49L), the occurrence of the disease was assessed in mice lacking T cells of either the 
ß or 
lineage (TCRß–/– or TCR–/–). TCR–/– mice were susceptible to CM, whereas all TCRß–/– mice were resistant, suggesting that T cells of the ß lineage are important in the genesis of CM. The repertoire of TCR Vß segment gene expression was examined by flow cytometry in B10.D2 mice, a strain highly susceptible to CM induced by infection with PbA 1.49L. In these mice, CM was associated with an increase of T cells bearing the Vß8.1, 2 segments in the peripheral blood lymphocytes. Most Vß8.1, 2+ T cells from peripheral blood lymphocytes of the mice that developed CM belonged to the CD8 subset, and exhibited the CD69+, CD44high and CD62Llow phenotype surface markers. The link between the increase in Vß8.1, 2+ T cells and the neuropathological consequences of PbA infection was strengthened by the observation that the occurrence of CM was significantly reduced in mice treated with KJ16 antibodies against the Vß8.1 and Vß8.2 chains, and in mice rendered deficient in Vß8.1+ T cells by a mouse mammary tumor virus superantigen.
Keywords: cerebral malaria, malaria pathogenesis, Plasmodium berghei ANKA, T cell response, TCR Vß gene expression
Transmitting editor: S. H. E. Kaufmann
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