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How do commensal gut bacteria coexist with the host without causing uncontrolled inflammation? The answer may lie in the induction of the association of PPAR-γ with NF-κB.
The immune system uses many sensors to detect and report microbial invaders. Most of these sensors are associated with immune cells, but the extracellular matrix also seems to be essential for this sentinel duty.
Murr1, a protein linked to copper homeostasis, is shown in a recent Nature paper to inhibit the degradation of IκBα. This unexpected action of Murr1, which blunts both basal and stimulus-coupled activation of the NF-κB transcription factor, is key in making resting CD4 T lymphocytes nonpermissive for HIV infection.
Dendritic cell–based vaccines have been rapidly transferred from the laboratory to the clinic. As the full potential of these cells has not yet been entirely exploited, many strategies could improve the immunogenicity of these vaccines.
