IL-17 metabolically reprograms activated fibroblastic reticular cells for proliferation and survival.

ABSTRACT: Lymph-node (LN) stromal cell populations expand during the inflammation that accompanies T cell activation. Interleukin-17 (IL-17)-producing helper T cells (T_H17 cells) promote inflammation through the induction of cytokines and chemokines in peripheral tissues. We demonstrate a critical requirement for IL-17 in the proliferation of LN and splenic stromal cells, particularly fibroblastic reticular cells (FRCs), during experimental autoimmune encephalomyelitis and colitis. Without signaling via the IL-17 receptor, activated FRCs underwent cell cycle arrest and apoptosis, accompanied by signs of nutrient stress in vivo. IL-17 signaling in FRCs was not required for the development of T_H17 cells, but failed FRC proliferation impaired germinal center formation and antigen-

SUBMITTER: Majumder S 

PROVIDER: S-EPMC6519710 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature