IL-10-producing, ST2-expressing Foxp3 + T cells in multiple sclerosis brain lesions.

Autor: Zandee SEJ; MRC Centre for Inflammation Research, The Edinburgh Centre for Multiple Sclerosis Research and Centre for Immunity Infection and Evolution, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK., O'Connor RA; MRC Centre for Inflammation Research, The Edinburgh Centre for Multiple Sclerosis Research and Centre for Immunity Infection and Evolution, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK., Mair I; MRC Centre for Inflammation Research, The Edinburgh Centre for Multiple Sclerosis Research and Centre for Immunity Infection and Evolution, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK., Leech MD; MRC Centre for Inflammation Research, The Edinburgh Centre for Multiple Sclerosis Research and Centre for Immunity Infection and Evolution, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK., Williams A; MRC Centre for Regenerative Medicine, The Edinburgh Centre for Multiple Sclerosis Research, University of Edinburgh, Edinburgh, UK., Anderton SM; MRC Centre for Inflammation Research, The Edinburgh Centre for Multiple Sclerosis Research and Centre for Immunity Infection and Evolution, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Jazyk: angličtina
Zdroj: Immunology and cell biology [Immunol Cell Biol] 2017 May; Vol. 95 (5), pp. 484-490. Date of Electronic Publication: 2017 Feb 07.
DOI: 10.1038/icb.2017.3
Abstrakt: CD4 + Foxp3 + T regulatory (Treg) cells provide a key defence against inflammatory disease, but also have an ability to produce pro-inflammatory cytokines. The evidence for these two possibilities in multiple sclerosis (MS) is controversial. However, this has largely been based on studies of circulating Treg cells derived from peripheral blood, rather than the central nervous system. We show that Foxp3 + cells in the brains of MS patients predominantly produce interleukin-10 (IL-10) and show high expression of the IL-33 receptor ST2 (associated with potent Treg function), indicating that Treg in the inflamed brain maintain their suppressive function.
Databáze: MEDLINE