Constitutive immune mechanisms: mediators of host defence and immune regulation

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisReviewForskningpeer review

DOI

  • Søren R. Paludan
  • Thomas Pradeu, CNRS, Universite de Bordeaux
  • ,
  • Seth L. Masters, Walter and Eliza Hall Institute of Medical Research, University of Melbourne
  • ,
  • Trine H. Mogensen

The immune system enables organisms to combat infections and to eliminate endogenous challenges. Immune responses can be evoked through diverse inducible pathways. However, various constitutive mechanisms are also required for immunocompetence. The inducible responses of pattern recognition receptors of the innate immune system and antigen-specific receptors of the adaptive immune system are highly effective, but they also have the potential to cause extensive immunopathology and tissue damage, as seen in many infectious and autoinflammatory diseases. By contrast, constitutive innate immune mechanisms, including restriction factors, basal autophagy and proteasomal degradation, tend to limit immune responses, with loss-of-function mutations in these pathways leading to inflammation. Although they function through a broad and heterogeneous set of mechanisms, the constitutive immune responses all function as early barriers to infection and aim to minimize any disruption of homeostasis. Supported by recent human and mouse data, in this Review we compare and contrast the inducible and constitutive mechanisms of immunosurveillance.

OriginalsprogEngelsk
TidsskriftNature Reviews Immunology
Vol/bind21
Nummer3
Sider (fra-til)137-150
Antal sider14
ISSN1474-1733
DOI
StatusUdgivet - mar. 2021

Bibliografisk note

Funding Information:
S.R.P. is funded by the European Research Council (ERC-AdG ENVISION; 786602), the Novo Nordisk Foundation (NNF18OC0030274) and the Lundbeck Foundation (R198-2015-171 and R268-2016-3927). T.P. is funded by the European Research Council (ERC-StG IDEM; 637647). S.L.M. acknowledges funding from a Howard Hughes Medical Institute–Wellcome International Research Scholarship and the Sylvia and Charles Viertel Foundation. T.H.M. received funding from Aarhus University Research Foundation (AUFF-E-215-FLS-8-66), the Danish Council for Independent Research-Medical Sciences (4004-00047B) and the Lundbeck Foundation (R268-2016-3927). The authors thank D. Olagnier for critical reading of the manuscript and comments and suggestions.

Publisher Copyright:
© 2020, Springer Nature Limited.

Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.

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