@article{TEXTUAL,
      recid = {11044},
      author = {Akkaya, Munir and Bansal, Abhisheka and Sheehan, Patrick  W. and Pena, Mirna and Molina-Cruz, Alvaro and Orchard,  Lindsey M. and Cimperman, Clare K. and Qi, Chen-Feng and  Ross, Philipp and Yazew, Takele and Sturdevant, Daniel and  Anzick, Sarah L. and Thiruvengadam, Girija and Otto, Thomas  Dan and Billker, Oliver and Llinás, Manuel and Miller,  Louis H. and Pierce, Susan K.},
      title = {A single-nucleotide polymorphism in a <i>Plasmodium  berghei</i> ApiAP2 transcription factor alters the  development of host immunity},
      journal = {Science Advances},
      address = {2020-02-05},
      number = {TEXTUAL},
      abstract = {The acquisition of malaria immunity is both remarkably  slow and unpredictable. At present, we know little about  the malaria parasite genes that influence the host’s  ability to mount a protective immune response. Here, we  show that a single-nucleotide polymorphism (SNP) resulting  in a single amino acid change (S to F) in an ApiAP2  transcription factor in the rodent malaria parasite  Plasmodium berghei (Pb) NK65 allowed infected mice to mount  a T helper cell 1 (TH1)–type immune response that  controlled subsequent infections. As compared to  PbNK65<sup>S</sup>, PbNK65<sup>F</sup> parasites  differentially expressed 46 genes, most of which are  predicted to play roles in immune evasion.  PbNK65<sup>F</sup> infections resulted in an early  interferon-γ response and a later expansion of germinal  centers, resulting in high levels of infected red blood  cell–specific T<sub>H</sub>1-type immunoglobulin G2b  (IgG2b) and IgG2c antibodies. Thus, the Pb ApiAP2  transcription factor functions as a critical parasite  virulence factor in malaria infections.},
      url = {http://knowledge.uchicago.edu/record/11044},
}