Research output: Contribution to journal › Article › peer-review
Michael Ridley, Veerle Fleskens, Ceri Roberts, Sylvine Lalnunhlimi, Aldana Asnesf, Aoife O'Byrne, Kathryn Steel, Giovanni Povoleri, Jonathan Sumner, Paul Lavender, Leonie Taams
Original language | English |
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Pages (from-to) | 2940-2948 |
Number of pages | 9 |
Journal | Journal of Immunology |
Volume | 204 |
Issue number | 11 |
Early online date | 22 Apr 2020 |
DOIs | |
Accepted/In press | 2 Apr 2020 |
E-pub ahead of print | 22 Apr 2020 |
Published | 1 Jun 2020 |
Additional links |
19-01283-FLR_R2_Taams 020420 for PURE
19_01283_FLR_R2_Taams_020420_for_PURE.pdf, 3.07 MB, application/pdf
Uploaded date:23 Apr 2020
Version:Accepted author manuscript
Licence:CC BY
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The expression of anti-inflammatory IL-10 by CD4 + T cells is indispensable for immune homeostasis, as it allows T cells to moderate their effector function. We previously showed that TNF-a blockade during T cell stimulation in CD4 + T cell/monocyte cocultures resulted in maintenance of IL-10–producing T cells and identified IKZF3 as a putative regulator of IL-10. In this study, we tested the hypothesis that IKZF3 is a transcriptional regulator of IL-10 using a human CD4 + T cell–only culture system. IL-10 + CD4 + T cells expressed the highest levels of IKZF3 both ex vivo and after activation compared with IL-10–CD4 + T cells. Pharmacological targeting of IKZF3 with the drug lenalidomide showed that IKZF3 is required for anti-CD3/CD28 mAb–mediated induction of IL-10 but is dispensable for ex vivo IL-10 expression. However, overexpression of IKZF3 was unable to upregulate IL-10 at the mRNA or protein level in CD4 + T cells and did not drive the transcription of the IL10 promoter or putative local enhancer constructs. Collectively, these data indicate that IKZF3 is associated with but not sufficient for IL-10 expression in CD4 + T cells.
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