Type I Interferon Sensitizes Lymphocytes to Apoptosis and Reduces Resistance to Listeria Infection
Copyright policy )Type I Interferon Sensitizes Lymphocytes to Apoptosis and Reduces Resistance to Listeria Infection
Infection with Listeria monocytogenes causes lymphocyte apoptosis that is mediated by the actions of the pore-forming virulence factor listeriolysin O (LLO). Previous work showed that activated lymphocytes were highly sensitive to LLO-induced apoptosis, whereas resting lymphocytes were less susceptible. We now show that mice deficient in the type I interferon (IFN) receptor were more resistant to Listeria infection and had less apoptotic lesions than wild-type counterparts. Furthermore, treatment of resting splenic lymphocytes with recombinant IFN-αA enhanced their susceptibility to LLO-induced apoptosis. Together, these data suggest that type I IFN signaling is detrimental to handling of a bacterial pathogen and may enhance the susceptibility of lymphocytes undergoing apoptosis in response to bacterial pore-forming toxins.
- Washington University in St. Louis School of Medicine United States
- University of Mary United States
- Washington University in St. Louis United States
- Washington University in St. Louis United States
CD4-Positive T-Lymphocytes, Bacterial Toxins, Brief Definitive Report, Apoptosis, Mice, Mutant Strains, Hemolysin Proteins, Mice, Interferon Type I, Medicine and Health Sciences, In Situ Nick-End Labeling, Animals, Eosine Yellowish-(YS), Listeriosis, Hematoxylin, Heat-Shock Proteins, Spleen, Receptors, Interferon, Signal Transduction
CD4-Positive T-Lymphocytes, Bacterial Toxins, Brief Definitive Report, Apoptosis, Mice, Mutant Strains, Hemolysin Proteins, Mice, Interferon Type I, Medicine and Health Sciences, In Situ Nick-End Labeling, Animals, Eosine Yellowish-(YS), Listeriosis, Hematoxylin, Heat-Shock Proteins, Spleen, Receptors, Interferon, Signal Transduction
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