Abstract
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.
Original language | English |
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Pages (from-to) | 535-540 |
Number of pages | 6 |
Journal | Journal of Experimental Medicine |
Volume | 200 |
Issue number | 4 |
DOIs | |
State | Published - Aug 16 2004 |
Keywords
- Apoptosis
- Cytokines
- Inflammation
- Listeria
- T lymphocytes