The protozoan Trypanosoma cruzi is the causative agent of Chagas' disease, which is characterized by severe immune suppression. The ability of T. cruzi to mediate immune suppression can be observed by culturing peripheral-blood T cells in the presence and in the absence of T. cruzi and then evaluating their immune reactivity. Antigen, mitogen, or anti-CD3 monoclonal antibody normally can activate peripheral T cells, but in the presence of T. cruzi, T cells are not activated by any of these agents. The defect in these lymphocytes has been traced to a dramatic reduction in the expression of the 55-kDa a subunit of the IL-2 receptor. As noted earlier, the high-affinity IL-2 receptor contains a, p, and 7 subunits. The a subunit is specific for cytokine binding (see Figure 12-9). Co-culturing of T cells with T. cruzi and subsequent staining with fluorescein-labeled anti-TAC, which binds to the a subunit, revealed a 90% decrease in the level of the a subunit.
Although the mechanism by which T. cruzi suppresses expression of the a subunit is still unknown, the suppression can be induced across a filter that prevents contact between the lymphocytes and protozoa. This finding suggests that a diffusible factor mediates suppression. Such a factor, once isolated, might have numerous clinical applications for regulating the level of activated T cells in leukemias and autoimmune diseases.
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