Edinburgh Research Explorer

Reciprocal Regulation of Lymphoid Tissue Development in the Large Intestine by IL-25 and IL-23: Regulation of colonic ILF by IL-25/IL-23

Research output: Contribution to journalArticle

Related Edinburgh Organisations

Open Access permissions



  • Download as Adobe PDF

    Rights statement: This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0

    Final published version, 7.16 MB, PDF document

Original languageEnglish
Pages (from-to)582-595
JournalMucosal Immunology
Issue number3
Early online date24 Sep 2014
Publication statusPublished - May 2015


Isolated lymphoid follicles (ILF) develop post-birth in the small and large intestines (SI and LI) and represent a dynamic response of the gut immune system to the microbiota. Despite their similarities, ILF development in the SI and LI differs on a number of levels. We show that unlike ILF in the SI, the microbiota inhibits ILF development as conventionalisation of germ-free mice reduced colonic ILF. From this, we identified a novel mechanism regulating colonic ILF development through the action of IL-25 on IL-23 and its ability to modulate Treg differentiation. Colonic ILF develop in the absence of a number of factors required for 30 the development of their SI counterparts and can be specifically suppressed by factors other than IL-25. However, IL-23 is the only factor identified that specifically promotes colonic ILF without affecting SI-ILF development. Both IL-23 and ILF are associated with inflammatory bowel disease, suggesting that disruption to this pathway may have an important role in the breakdown of microbiota-immune homeostasis.

Download statistics

No data available

ID: 16625619