Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Aug 7;10(8):e1004252.
doi: 10.1371/journal.ppat.1004252. eCollection 2014 Aug.

Disruption of fas-fas ligand signaling, apoptosis, and innate immunity by bacterial pathogens

Adam J Caulfield  1 , Wyndham W Lathem  1
Affiliations
Review

Disruption of fas-fas ligand signaling, apoptosis, and innate immunity by bacterial pathogens

Adam J Caulfield et al. PLoS Pathog. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Disruption of Fas-FasL signaling by Pla of Y. pestis and NleB of EPEC.
In response to bacterial infections, the host attempts to induce Fas/FasL-dependent cell apoptosis. During pneumonic plague, however, the Pla protease of Y. pestis directly cleaves FasL on effector cells to prevent the initiation of Fas signaling, blocking the activation of the initiator caspase-8, effector caspases -3 and -7, and cell death by apoptosis. As an alternative strategy during gastrointestinal infection, EPEC injects the type-III-secreted effector NleB into the cytoplasm of target cells, where it modifies FADD with N-acetylglucosamine to prevent death domain binding and downstream signaling following the engagement of Fas by FasL. While the mechanisms by which these bacteria target Fas-FasL signaling are distinct, the end result is the same: inhibition of apoptosis.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Suda T, Takahashi T, Golstein P, Nagata S (1993) Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family. Cell 75: 1169–1178. - PubMed
    1. Locksley RM, Killeen N, Lenardo MJ (2001) The TNF and TNF receptor superfamilies: integrating mammalian biology. Cell 104: 487–501. - PubMed
    1. Strasser A, Jost PJ, Nagata S (2009) The many roles of FAS receptor signaling in the immune system. Immunity 30: 180–192. - PMC - PubMed
    1. Wang L, Yang JK, Kabaleeswaran V, Rice AJ, Cruz AC, et al. (2010) The Fas-FADD death domain complex structure reveals the basis of DISC assembly and disease mutations. Nat Struct Mol Biol 17: 1324–1329. - PMC - PubMed
    1. Nagata S (1997) Apoptosis by death factor. Cell 88: 355–365. - PubMed