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Role of gamma interferon during infection with Plasmodium chabaudi chabaudi
S J Meding1, S C Cheng, B Simon-Haarhaus
1Max-Planck-Institut für Immunbiologie, Freiburg, Federal Republic of Germany.
Abstract:
A role has been proposed for inflammatory mediators such as gamma interferon (IFN-gamma) and reactive oxygen intermediates in the control of the blood stages of Plasmodium organisms. It was previously shown that IFN-gamma can be detected in the plasma of mice with a primary infection by Plasmodium chabaudi chabaudi (AS). We found that susceptible and other resistant mouse strains produced IFN-gamma, suggesting that susceptibility is not due to a defect in IFN-gamma production. Administration of IFN-gamma to intact C57BL/6 mice slightly decreased and partially delayed parasitemia, whereas in vivo depletion of IFN-gamma through injection of a "cocktail" of monoclonal antibodies against IFN-gamma exacerbated infection. Since CD4+ T cells are essential for the development of a protective immune response to P. chabaudi chabaudi, we tested whether CD4+ T cells are responsible for IFN-gamma production in vivo and whether exogenous IFN-gamma can replace the protective function of the CD4+ T cells. Mice depleted of CD4+ T cells were unable to produce IFN-gamma, but factors in addition to IFN-gamma may be important in parasite clearance.
Insights
Gamma interferon (IFN-gamma) plays a role in controlling Plasmodium chabaudi chabaudi infections. While CD4+ T cells are crucial for IFN-gamma production, other factors may also aid parasite clearance.
Area of Science:
- Immunology
- Parasitology
- Infectious Diseases
Background:
- Inflammatory mediators like gamma interferon (IFN-gamma) are implicated in controlling Plasmodium parasite blood stages.
- IFN-gamma is detectable in mice during Plasmodium chabaudi chabaudi (AS) infection.
- Susceptibility to infection is not linked to a deficiency in IFN-gamma production.
Purpose of the Study:
- To investigate the role of IFN-gamma in Plasmodium chabaudi chabaudi (AS) infection control.
- To determine if CD4+ T cells are the primary source of in vivo IFN-gamma production.
- To assess if exogenous IFN-gamma can substitute for the protective function of CD4+ T cells.
Main Methods:
- Measuring IFN-gamma levels in plasma of infected mice.
- Administering IFN-gamma to intact mice and observing parasitemia.
- Depleting IFN-gamma in vivo using monoclonal antibodies.
- Depleting CD4+ T cells and assessing IFN-gamma production and infection outcomes.
Main Results:
- Administration of IFN-gamma showed a modest decrease and delay in parasitemia.
- In vivo depletion of IFN-gamma worsened the infection.
- Mice depleted of CD4+ T cells failed to produce IFN-gamma.
- CD4+ T cells are essential for IFN-gamma production during infection.
Conclusions:
- IFN-gamma contributes to controlling Plasmodium chabaudi chabaudi (AS) blood-stage infection.
- CD4+ T cells are critical for generating IFN-gamma during infection.
- Additional factors beyond IFN-gamma are likely involved in parasite clearance.