Affiliation:
1. Department of Microbiology, University of Chicago, Chicago, Illinois, USA
Abstract
Caspase-3 controls the apoptotic pathway, a form of programmed cell death designed to be immunologically silent. Polymorphisms leading to reduced caspase-3 activity are associated with variable effects on tumorigenesis and yet arise frequently.
Staphylococcus aureus
is a human commensal and a frequent cause of soft tissue and bloodstream infections. Successful commensalism and virulence can be explained by the secretion of a plethora of immune evasion factors. One such factor, AdsA, destroys phagocytic cells by exploiting the apoptotic pathway. However, human
CASP3
variants with loss-of-function alleles shield phagocytes from AdsA-mediated killing. This finding raises the possibility that some caspase-3 alleles may arise from exposure to
S. aureus
and other human pathogens that exploit the apoptotic pathway for infection.
Funder
HHS | NIH | National Institute of Allergy and Infectious Diseases
Deutsche Forschungsgemeinschaft
Publisher
American Society for Microbiology
Cited by
37 articles.
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