Morris O. MakobongoGeorge RidingHuji XuChakrit HirunpetcharatDianne KeoughJohn De JerseyPeter WilladsentMichael F. GoodRoyal Brisbane HospitalGehrmann LabsUniversity of QueenslandMahidol University2018-07-242018-07-242003-03-04Proceedings of the National Academy of Sciences of the United States of America. Vol.100, No.5 (2003), 2628-2633002784242-s2.0-0345701295https://repository.li.mahidol.ac.th/handle/20.500.14594/21050Although there is good evidence that Immun. to the blood stages of malaria parasites can be mediated by different effector components of the adaptive immune system, target antigens for a Prin. component, effector CD4+ T cells, have never been defined. We generated CD4+ T cell lines to fractions of native antigens from the blood stages of the rodent parasite, Plasmodium yoelii,/identified fraction-specific T cells that had a Th1 phenotype (producing IL-2, IFN-γ, and tumor necrosis factor-α, but not IL-4, after antigenic stimulation). These T cells could inhibit parasite growth in recipient severe combined immunodeficient mice. N-terminal sequencing of the fraction showed identity with hypoxanthine guanine xanthine phosphoribosyl transferase (HGXPRT). Recombinant HGXPRT from the human malaria parasite, Plasmodium falciparum, activated the T cells in vitro, and immunization of normal mice with recombinant HGXPRT reduced parasite growth rates in all mice after challenge.Mahidol UniversityMultidisciplinaryArticleSCOPUS10.1073/pnas.0337629100