Cellular and Molecular Life Sciences

, Volume 67, Issue 10, pp 1643–1651

Control of infection by pyroptosis and autophagy: role of TLR and NLR

Multi-author Review

DOI: 10.1007/s00018-010-0335-5

Cite this article as:
Bortoluci, K.R. & Medzhitov, R. Cell. Mol. Life Sci. (2010) 67: 1643. doi:10.1007/s00018-010-0335-5


Cells can die by distinct mechanisms with particular impacts on the immune response. In addition to apoptosis and necrosis, recent studies lead to characterization of a new pro-inflammatory form of cell death, pyroptosis. TLR and NLR, central innate immune sensors, can control infections by modulating host cell survival. In addition, TLRs can promote the induction of autophagy, thus promoting delivery of infecting pathogens to the lysosomes. On the other hand, activation of some NLR members, especially NLRC4 and NAIP5, leads to the infected cell death by pyroptosis, which is accompanied by secretion of the pro-inflammatory cytokines IL-1β, IL-18, and IL-33. Data presented here illustrate how the compartmentalization of the innate immune sensors can influence the outcome of infections by controlling the fate of host cells.


TLR NLR Pyroptosis Autophagy Cell death Inflammasomes 

Copyright information

© Springer Basel AG 2010

Authors and Affiliations

  1. 1.Department of Biological SciencesFederal University of São Paulo-Campus DiademaDiademaBrazil
  2. 2.Department of Immunology, Institute of Biomedical SciencesUniversity of São PauloSão PauloBrazil
  3. 3.Howard Hughes Medical InstituteChevy ChaseUSA
  4. 4.Department of ImmunobiologyYale University School of MedicineNew HavenUSA

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