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Inflammation suppressor genes: please switch out all the lights
Author(s) -
Wells Christine A.,
Ravasi Timothy,
Hume David A.
Publication year - 2005
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1204710
Subject(s) - biology , inflammation , suppressor , immune system , socs2 , gene , immunology , population , genetics , microbiology and biotechnology , demography , sociology
An effective immune system requires rapid and appropriate activation of inflammatory mechanisms but equally rapid and effective resolution of the inflammatory state. A review of the canonical host response to gram‐negative bacteria, the lipopolysaccharide‐Toll‐like receptor 4 signaling cascade, highlights the induction of repressors that act at each step of the activation process. These inflammation suppressor genes are characterized by their induction in response to pathogen, typically late in the macrophage activation program, and include an expanding class of dominant‐negative proteins derived from alternate splicing of common signaling components. Despite the expanse of anti‐inflammatory mechanisms available to an activated macrophage, the frailty of this system is apparent in the large numbers of genes implicated in chronic inflammatory diseases. This apparent lack of redundancy between inflammation suppressor genes is discussed with regard to evolutionary benefits in generating a heterogeneous population of immune cells and consequential robustness in defense against new and evolving pathogens.