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Control of Trypanosoma cruzi infection in mice deprived of T-cell help
M E Rottenberg1, D A Rodriguez, A Orn
1Department of Immunology, Karolinska Institute, Stockholm, Sweden.
Abstract:
The role of CD4+ T lymphocytes in the resistance of BALB/c mice to Trypanosoma cruzi was examined by in vivo depletion using monoclonal anti-CD4 antibodies (MoAbs). When the administration of MoAbs was initiated 2 days before, or 5 to 12 days after the infection (dpi) with 50 bloodstream-form trypomastigotes of the Tulahuén strain, mice showed an enhanced susceptibility to the parasite. Specific IgG, but not IgM responses, were inhibited in anti-CD4-treated and infected mice. However, when anti-CD4 treatment of mice was delayed until the 8th week of infection, neither a reactivation of the infection as determined by mortality or parasitaemia, nor a modulation of the titre of anti-T. cruzi IgG antibodies was detected. Furthermore, mice chronically infected with T. cruzi and deprived of CD4+ T cells resisted the challenge with 50,000 trypomastigotes (approximately 1000 LD50). Secondary antibody responses against parasite antigens were inhibited after in vitro depletion of CD4+ cells in chronically infected mice before boosting with T. cruzi antigens. However, recipients of CD4 or T-cell-depleted spleen cells from mice chronically infected with T. cruzi were protected when challenged with the parasite. The possibility that the parasite control is maintained by long-lived B cells capable of rapid differentiation into IgG-secreting plasma cells in the absence of T helper cells is discussed considering the present data.
Insights
CD4+ T cells are crucial for controlling Trypanosoma cruzi infection in mice. Depleting these cells early increases susceptibility, but chronic infection control may involve long-lived B cells.
Area of Science:
- Immunology
- Parasitology
- Infectious Diseases
Background:
- Trypanosoma cruzi causes Chagas disease, a significant global health concern.
- The role of CD4+ T lymphocytes in mediating resistance against T. cruzi infection is not fully understood.
Purpose of the Study:
- To investigate the role of CD4+ T lymphocytes in BALB/c mice's resistance to Trypanosoma cruzi infection.
- To determine the impact of CD4+ T cell depletion on susceptibility, antibody responses, and long-term control of T. cruzi infection.
Main Methods:
- In vivo depletion of CD4+ T lymphocytes using anti-CD4 monoclonal antibodies (MoAbs) at various time points relative to infection.
- Assessment of parasite susceptibility, mortality, parasitemia, and specific antibody responses (IgG, IgM).
- Evaluation of protection against secondary challenge in chronically infected, T-cell-depleted mice and recipients of spleen cells.
Main Results:
- Early depletion of CD4+ T cells (before or shortly after infection) significantly increased susceptibility to T. cruzi.
- Anti-CD4 treatment inhibited specific IgG antibody responses but did not cause reactivation or alter antibody titers in chronically infected mice.
- Chronically infected mice depleted of CD4+ T cells resisted a high-dose challenge, suggesting alternative parasite control mechanisms.
Conclusions:
- CD4+ T lymphocytes play a critical role in the initial control of Trypanosoma cruzi infection.
- Long-lived B cells may contribute to sustained parasite control in the absence of T helper cells during chronic infection.
- These findings highlight the complex interplay between T cell-dependent and independent mechanisms in immunity to T. cruzi.
