A TNF-p100 pathway subverts noncanonical NF-κB signaling in inflamed secondary lymphoid organs.

ABSTRACT: Lymphotoxin-beta receptor (LTβR) present on stromal cells engages the noncanonical NF-κB pathway to mediate RelB-dependent expressions of homeostatic chemokines, which direct steady-state ingress of naïve lymphocytes to secondary lymphoid organs (SLOs). In this pathway, NIK promotes partial proteolysis of p100 into p52 that induces nuclear translocation of the RelB NF-κB heterodimers. Microbial infections often deplete homeostatic chemokines; it is thought that infection-inflicted destruction of stromal cells results in the downregulation of these chemokines. Whether inflammation per se also regulates these processes remains unclear. We show that TNF accumulated upon non-infectious immunization of mice similarly downregulates the expressions of these chemokines and consequently dimi

SUBMITTER: Mukherjee T 

PROVIDER: S-EPMC5709727 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature