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Regulates Proinflammatory Cytokine Production and Determines the Outcome of Lethal and Nonlethal Plasmodium yoelii Infections 1
* Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom; and
Department of Immunology and Molecular Pathology, Royal Free and University College, London Medical School, London, United Kingdom
Transforming growth factor-
is an essential moderator of malaria-induced inflammation in mice. In this study, we show that the virulence of malaria infections is dependent upon the cellular source of TGF- and the timing of its production. C57BL/6 mice infected with a nonlethal (Py17X) strain of Plasmodium yoelii produce TGF- from 5 days postinfection; this correlates with resolution of parasitemia, down-regulation of TNF-
, and full recovery. In contrast, infection with the lethal strain Py17XL induces high levels of circulating TGF- within 24 h; this is associated with delayed and blunted IFN-
and TNF- responses, failure to clear parasites, and 100% mortality. Neutralization of early TGF- in Py17XL infection leads to a compensatory increase in IL-10 production, while simultaneous neutralization of TGF- and IL-10R signaling leads to up-regulation of TNF- and IFN-, prolonged survival in all, and ultimate resolution of infection in 40% of Py17XL-infected animals. TGF- production can be induced in an Ag-specific manner from splenocytes of infected mice, and by cross-linking surface CTLA-4. CD25+ and CD8+ cells are the primary source of TGF- following Py17X stimulation of splenocytes, whereas Py17XL induces significant production of TGF- from adherent cells. In mice immunized against Py17XL, the early TGF- response is inhibited and is accompanied by significant up-regulation of IFN- and TNF- and rapid resolution of challenge infections.
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