Journal
NATURE IMMUNOLOGY
Volume 20, Issue 4, Pages 458-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41590-019-0350-0
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Funding
- Hoffmann la Roche
- Kidney Research UK
- National Health and Medical Research Council of Australia
- Versus Arthritis Career Development Fellowship [20305]
- Systems Immunity University Research Institute at Cardiff
- Rutherford Fellowship Grant
- Medical Research Council [36661, 20022]
- Wellcome Trust Investigator Award
- UK Dementia Research Institute [107964/Z/15/Z]
- Systems Immunity University Research Institute in Cardiff
- MRC [G0800648, UKDRI-3001] Funding Source: UKRI
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The cytokine IL-6 controls the survival, proliferation and effector characteristics of lymphocytes through activation of the transcription factors STAT1 and STAT3. While STAT3 activity is an ever-present feature of IL-6 signaling in CD4(+) T cells, prior activation via the T cell antigen receptor limits IL-6's control of STAT1 in effector and memory populations. Here we found that phosphorylation of STAT1 in response to IL-6 was regulated by the tyrosine phosphatases PTPN2 and PTPN22 expressed in response to the activation of naive CD4(+) T cells. Transcriptomics and chromatin immunoprecipitation-sequencing (ChIP-seq) of IL-6 responses in naive and effector memory CD4(+) T cells showed how the suppression of STAT1 activation shaped the functional identity and effector characteristics of memory CD4(+) T cells. Thus, tyrosine phosphatases induced by the activation of naive T cells determine the way activated or memory CD4(+) T cells sense and interpret cytokine signals.
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