T-Cell-Dependent Control of Acute Giardia lamblia Infections in Mice

SM Singer, TE Nash - Infection and immunity, 2000 - Am Soc Microbiol
SM Singer, TE Nash
Infection and immunity, 2000Am Soc Microbiol
We have studied immune mechanisms responsible for control of acute Giardia lamblia and
Giardia muris infections in adult mice. Association of chronic G. lamblia infection with
hypogammaglobulinemia and experimental infections of mice with G. muris have led to the
hypothesis that antibodies are required to control these infections. We directly tested this
hypothesis by infecting B-cell-deficient mice with either G. lamblia or G. muris. Both wild-type
mice and B-cell-deficient mice eliminated the vast majority of parasites between 1 and 2 …
Abstract
We have studied immune mechanisms responsible for control of acuteGiardia lamblia and Giardia muris infections in adult mice. Association of chronic G. lamblia infection with hypogammaglobulinemia and experimental infections of mice withG. muris have led to the hypothesis that antibodies are required to control these infections. We directly tested this hypothesis by infecting B-cell-deficient mice with either G. lamblia or G. muris. Both wild-type mice and B-cell-deficient mice eliminated the vast majority of parasites between 1 and 2 weeks postinfection with G. lamblia. G. muris was also eliminated in both wild-type and B-cell-deficient mice. In contrast, T-cell-deficient and scid mice failed to controlG. lamblia infections, as has been shown previously forG. muris. Treatment of wild-type or B-cell-deficient mice with antibodies to CD4 also prevented elimination of G. lamblia, confirming a role for T cells in controlling infections. By infecting mice deficient in either αβ- or γδ-T-cell receptor (TCR)-expressing T cells, we show that the αβ-TCR-expressing T cells are required to control parasites but that the γδ-TCR-expressing T cells are not. Finally, infections in mice deficient in production of gamma interferon or interleukin 4 (IL-4) and mice deficient in responding to IL-4 and IL-13 revealed that neither the Th1 nor the Th2 subset is absolutely required for protection fromG. lamblia. We conclude that a T-cell-dependent mechanism is essential for controlling acute Giardia infections and that this mechanism is independent of antibody and B cells.
American Society for Microbiology