Abstract
Anthrax edema toxin (ET), a powerful adenylyl cyclase, is an important virulence factor of Bacillus anthracis. Until recently, only a modest amount of research was performed to understand the role this toxin plays in the organism’s immune evasion strategy. A new wave of studies have begun to elucidate the effects this toxin has on a variety of host cells. While efforts have been made to illuminate the effect ET has on cells of the adaptive immune system, such as T cells, the greatest focus has been on cells of the innate immune system, particularly the macrophage. Here we discuss the immunoevasive activities that ET exerts on macrophages, as well as new research on the effects of this toxin on B cells.
Highlights
Anthrax is an asynchronous, toxin-mediated disease caused by a gram-positive bacterium, Bacillus anthracis
Differing culture conditions and concentrations of edema factor (EF) and protective antigen (PA) have been used in various studies across the literature, it appears that the intensity and duration of the cAMP response generated by edema toxin (ET) varies between cell types
In vitro studies with various host immune cell types performed in recent years have contributed to our overall knowledge of the immunosuppressive and immunodeviation strategies of ET
Summary
Toxin-mediated disease caused by a gram-positive bacterium, Bacillus anthracis. Macrophages were once presumed to be the primary mode of transport of spores/bacilli to the mediastinal lymph nodes, a recent publication has provided convincing evidence that DCs are the true ―Trojan Horse‖ of the organism [12]. Edema factor (EF) is a calcium- and calmodulin-dependent adenylyl cyclase [20] that converts ATP to cAMP with 1000-fold more activity than host adenylyl cyclases [21,22,23]. We present new data illustrating the effects of ET on B cell functions that are crucial to the development of an adaptive immune response in the host
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