At the crossway of ER-stress and proinflammatory responses - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue FEBS Journal Année : 2019

At the crossway of ER-stress and proinflammatory responses

Résumé

Immune cells detect specific microbes or damage to tissue integrity in order to initiate efficient immune responses. Abnormal accumulation of proteins in the endoplasmic reticulum (ER) can be seen as a sign of cellular malfunction and stress that triggers a collection of conserved emergency rescue programs. These different signaling cascades, which favor ER proteostasis and promote cell survival, are collectively known as the unfolded protein response (UPR). In recent years, a synergy between the UPR and inflammatory cytokine production has been unraveled, with different branches of the UPR entering in a cross-talk with specialized microbe sensing pathways, which turns on or amplify inflammatory cytokines production. Complementary to this synergetic activity, UPR induction alone, can itself be seen as a danger signal, and triggers directly or indirectly inflammation in different cellular and pathological models, this independently of the presence of pathogens. Here, we discuss recent advances on the nature of these cross-talks and how innate immunity, metabolism dysregulation, and ER-signaling pathways intersect in specialized immune cells, such as dendritic cells (DCs), and contribute to the pathogenesis of inflammatory diseases.

Domaines

Immunologie

Dates et versions

hal-02359462 , version 1 (12-11-2019)

Identifiants

Citer

Marisa Reverendo, Andreia Mendes, Rafael J. Arguello, Evelina Gatti, Philippe Pierre. At the crossway of ER-stress and proinflammatory responses. FEBS Journal, 2019, 286 (2, SI), pp.297-310. ⟨10.1111/febs.14391⟩. ⟨hal-02359462⟩

Collections

CNRS UNIV-AMU FRM
29 Consultations
0 Téléchargements

Altmetric

Partager

Gmail Mastodon Facebook X LinkedIn More