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. Author manuscript; available in PMC: 2018 Feb 6.
Published in final edited form as: Curr Opin Immunol. 2010 Feb;22(1):55–62. doi: 10.1016/j.coi.2010.01.003

Figure 3.

Figure 3

Proposed physiological and pathological outcomes of innate recognition of apoptotic cells dying from infection. When cells undergo apoptosis as a result of infection, the inflammatory trigger presented to the innate immune system is that of both infection and tissue injury. While PAMPs trigger inflammatory PRRs such as TLRs, apoptotic ‘eat-me’ signals trigger anti-inflammatory signaling pathways. Given that apoptosis frequently occurs during infection, the ability of the immune system to mount an effective response against pathogens despite the presence of immunosuppressive dying cells has been a long-standing paradox. A TH17 adaptive immune response reconciles the tolerance induced by apoptotic cell clearance with the necessarily inflammatory nature of infections. Through the release of inflammatory and reparative cytokines, TH17 cells can initiate not only defense against the pathogen, but also repair of injured tissues. Because one of the signals that trigger TH17 immunity consists of dying host cells, the pathological consequences of innate recognition of apoptotic cells during infection could be the development of autoimmunity.