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. 2018 Nov 13;9:2590. doi: 10.3389/fimmu.2018.02590

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Copyright © 2018 Bouras, Asehnoune and Roquilly.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Migratory dendritic cell response during primary pneumonia, and during sepsis-induced immunosuppression (left). The stimulation of immature migratory dendritic cells (im.DCs) by pathogen-associated molecular patterns induces the production of inflammatory cytokines (such as Interleukin-12) which stimulate innate-like lymphocyte and natural killer cell (NK) functions and primes naive CD4 T cells. During sepsis-induced immunosuppression (middle and right panels), bacterial clearance is decreased as compared to what is observed during primary pneumonia. (middle) Early after primary infection, activated DCs (Act.DCs) are unable to respond to subsequent pathogens, and fail to produce cytokines and prime new CD4 T cells. (right) Lately, newly formed DCs locally acquire a tolerogenic programing (Tol. DCs) upon instruction by local tolerogenic mediators (star). Glucocorticoid (GC) inhibits DC activation and limit the SIRS. Upon stimulation by pathogens, Tol-DCs do not activate NK cells but induce the local accumulation of Treg cells. GC inhibits tolerogenic mediators and can restore immunogenic functions of newly formed DCs.