FIGURE 19-11 Activation of eosinophils to kill helminths. IL-5 secreted by TH2 cells enhances the ability of helminths to kill the parasites. Crosslinking FceRl on eosinophils by IgE bound to helminth antigens may also induce eosinophil degranulation, releasing enzymes toxic to the parasites.
Chapter 10). The activities of IL-4 and IL-13 in IgE production and IL-5 in eosinophil activation contribute to a coordinated defense against helminths. In addition, IgE-dependent mast cell activation in the gastrointestinal tract promotes the expulsion of parasites by increasing peristalsis and by an outpouring of mucus. Studies in mice have highlighted the beneficial roles of IgE and mast cells. For example, mice treated with anti-IL-4 antibody and IL-4 knockout mice do not make IgE and appear to be more susceptible than normal animals to some helminthic infections. IL-5 knockout mice, which are unable to activate eosinophils, also show increased susceptibility to some helminths. Furthermore, genetically mast cell-deficient mice show increased susceptibility to infection by tick larvae, and immunity can be provided to these mice by adoptive transfer of specific IgE and mast cells (but not by either component alone). The larvae are eradicated by the late-phase reaction.
Mast cells play an important protective role as part of the innate immune response to bacterial infections.
Studies in mice have indicated that mast cells can be activated by IgE-independent mechanisms in the course of an acute bacterial infection and that the mediators they release are critical for clearing the infection. Mast cell-deficient mice are less capable of clearing and are more likely to die of acute bacterial infection of the peritoneum than are normal mice. The protective role of mast cells in this setting is mediated by TNF and depends on TNF-stimulated influx of neutrophils into the peritoneum, specifically, the late-phase reaction. The mechanisms by which mast cells are activated during innate immune responses to bacterial infection are not known but may involve complement activation by the alternative pathway, leading to the release of C5a, which directly triggers mast cell degranulation. It is also possible that the classical pathway of complement could be activated by natural antibodies that are produced by B-1 B cells and that recognize common microbial pathogens. Bacterial products may also activate mast cells by binding to Tolllike receptors expressed by the mast cells.
Mast cell-derived proteases have been shown to destroy some snake and insect venoms in mice. This is an unusual form of "innate immunity" against a potentially lethal encounter with nonmicrobial organisms.
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