Publications & Reports

Blood-stage Plasmodium berghei infection generates a potent, specific CD8+ T-cell response despite residence largely in cells lacking MHC I processing machinery.

Lau LS, Fernandez Ruiz D, Davey GM, de Koning-Ward TF, Papenfuss AT, Carbone FR, Brooks AG, Crabb BS, Heath WR
Department of Microbiology and Immunology, University of Melbourne, Parkville, Australia.

Abstract

Murine cerebral malaria is a complex disease caused by Plasmodium berghei ANKA infection. Several cell types, including CD8(+) T cells, are essential effectors of disease. Although the use of transgenic parasites expressing model antigens has revealed the induction of cytotoxic T lymphocytes (CTL) specific for these model antigens, there is no direct evidence for a response to authentic blood-stage parasite antigens, nor any knowledge of its magnitude. Our studies show that there is a dramatic primary parasite-specific CTL response, akin to viral immunity, reaching approximately 30% of splenic CD8(+) T cells, with many producing interferon-gamma and tumor necrosis factor-alpha. These cells express granzyme B and other markers of specific responders, are cytolytic, and respond to a broad array of major histocompatibility complex (MHC) I-restricted epitopes, 5 of which are identified here. Our studies indicate that vigorous CTL responses can be induced to pathogens even when they largely reside in red blood cells, which lack MHC I processing machinery.

Publication

  • Journal: The Journal of Infectious Diseases
  • Published: 15/12/2011
  • Volume: 204
  • Issue: 12
  • Pagination: 1989-1996

Health Issue