IL-10-producing, ST2-expressing Foxp3+T cells in multiple sclerosis brain lesions.
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.
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.
Stephanie Elizabeth Johanna
SEJ
Zandee
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.
Richard Anthony
RA
O'Connor
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.
Iris
I
Mair
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.
Melanie Dawn
MD
Leech
MRC Centre for Regenerative Medicine, The Edinburgh Centre for Multiple Sclerosis Research, University of Edinburgh, Edinburgh, UK.
Anna
A
Williams
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.
Stephen Mark
SM
Anderton
D000818:Animals; D001921:Brain / Q000473:pathology*; D015704:CD4 Antigens / Q000378:metabolism; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism*; D006801:Humans; D000072179:Interleukin-1 Receptor-Like 1 Protein / Q000378:metabolism*; D016753:Interleukin-10 / Q000096:biosynthesis*; D008810:Mice, Inbred C57BL; D009103:Multiple Sclerosis / Q000276:immunology* / Q000473:pathology*; D050378:T-Lymphocytes, Regulatory; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D015704:CD4 Antigens; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C079241:IL1RL1 protein, human; D000072179:Interleukin-1 Receptor-Like 1 Protein; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10