Acute infection with
Trypanosoma cruzi
results in intense myocarditis, which progresses to a chronic, asymptomatic
indeterminate form. The evolution toward this chronic cardiac form occurs in approximately 30% of all cases of
T. cruzi infection. Suppression of delayed type hypersensitivity (DTH) has been proposed as a potential explanation of
the indeterminate form. We investigated the effect of cyclophosphamide (CYCL) treatment on the regulatory mechanism
of DTH and the participation of heart interstitial dendritic cells (IDCs) in this process using BALB/c mice chronically
infected with T. cruzi. One group was treated with CYCL (20 mg/kg body weight) for one month. A DTH skin test was
performed by intradermal injection of
T. cruzi antigen (3 mg/mL) in the hind-footpad and measured the skin thickness
after 24 h, 48 h and 72 h. The skin test revealed increased thickness in antigen-injected footpads, which was more
evident in the mice treated with CYCL than in those mice that did not receive treatment. The thickened regions were
characterised by perivascular infiltrates and areas of necrosis. Intense lesions of the myocardium were present in
three/16 cases and included large areas of necrosis. Morphometric evaluation of lymphocytes showed a predominance
of TCD8 cells. Heart IDCs were immunolabelled with specific antibodies (CD11b and CD11c) and
T. cruzi antigens
were detected using a specific anti-
T. cruzi antibody. Identification of
T. cruzi antigens, sequestered in these cells using
specific anti-
T. cruzi antibodies was done, showing a significant increase in the number of these cells in treated mice.
These results indicate that IDCs participate in the regulatory mechanisms of DTH response to
T. cruzi infection.
