IL-27 promotes pathogenic T cells in a mouse model of Sjögren's disease

Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 264(2024) vom: 15. Juli, Seite 110260
Auteur principal: Debreceni, Ivy L (Auteur)
Autres auteurs: Barr, Jennifer Y, Upton, Ellen M, Chen, Yi-Guang, Lieberman, Scott M
Format: Article en ligne
Langue:English
Publié: 2024
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Exhausted CD8 T cells IL-27 Sjögren's disease T follicular cytotoxic cells T follicular helper cells T peripheral helper cells Il27 protein, mouse Interleukins Programmed Cell Death 1 Receptor plus... Receptors, Interleukin Interleukin-27 Inducible T-Cell Co-Stimulator Protein Apyrase EC 3.6.1.5 Il27ra protein, mouse Pdcd1 protein, mouse
Description
Résumé:Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.
Sjögren's disease (SjD) is a chronic autoimmune disease characterized by focal lymphocytic inflammation in lacrimal and salivary glands. We recently identified IL-27 as a requisite signal for the spontaneous SjD-like manifestations in nonobese diabetic (NOD) mice. Here, we define T cell-intrinsic effects of IL-27 in lacrimal gland disease in NOD mice. IL-27 receptor was required by both CD4 T effector (Te) cells and CD8 T cells to mediate focal inflammation. Intrinsic IL-27 signaling was associated with PD-1 and ICOS expressing T follicular helper (Tfh)-like CD4 Te cells within lacrimal glands, including subsets defined by CD73 or CD39 expression. CD8 T cells capable of IL-27 signaling also expressed PD-1 with subsets expressing ICOS and CD73 demonstrating a T follicular cytotoxic (Tfc)-like cell phenotype and others expressing a CD39hi exhausted-like phenotype. These findings suggest IL-27 is a key early signal driving a follicular-type response in lacrimal gland inflammation in NOD mice
Description:Date Completed 14.06.2024
Date Revised 27.06.2024
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2024.110260