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Chronic inflammation has been proposed as a driver of clonal evolution in myeloproliferative neoplasms (\n                    <jats:styled-content style=\"fixed-case\">MPN<\/jats:styled-content>\n                    ), suggesting that T cells play an important role in their pathogenesis. Treatment with\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    inhibitors (\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    i) results in improvements in\n                    <jats:styled-content style=\"fixed-case\">MPN<\/jats:styled-content>\n                    \u2010associated constitutional symptoms as well as reductions in splenomegaly. However, effects of\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    i on T cells in\n                    <jats:styled-content style=\"fixed-case\">MPN<\/jats:styled-content>\n                    are not well established and the baseline immune signature remains unclear. We investigated the frequency and function of\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    4\n                    <jats:sup>+<\/jats:sup>\n                    T cell subsets in 50\n                    <jats:styled-content style=\"fixed-case\">MPN<\/jats:styled-content>\n                    patients at baseline as well as during treatment with either ruxolitinib or fedratinib in a subset. We show that\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    4\n                    <jats:sup>+<\/jats:sup>\n                    \u00a0\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    127\n                    <jats:sup>low<\/jats:sup>\n                    \u00a0\n                    <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>\n                    25\n                    <jats:sup>high<\/jats:sup>\n                    \u00a0\n                    <jats:styled-content style=\"fixed-case\">FOXP<\/jats:styled-content>\n                    3\n                    <jats:sup>+<\/jats:sup>\n                    T regulatory cells are reduced in\n                    <jats:styled-content style=\"fixed-case\">MPN<\/jats:styled-content>\n                    patients compared to healthy controls and that this decrease is even more pronounced following\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    i therapy. Moreover, we show that after 6\u00a0months of treatment the number of T helper (Th)\u201017 cells increased. We also describe a functional \u2018silencing\u2019 of T helper cells both\n                    <jats:italic>in\u00a0vivo<\/jats:italic>\n                    and\n                    <jats:italic>in\u00a0vitro<\/jats:italic>\n                    and a blockade of pro\u2010inflammatory cytokines from these cells. This profound effect of\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    i on T cell function may underlay augmented rates of atypical infections that have been reported with use of these drugs.\n                  <\/jats:p>","DOI":"10.1111\/bjh.13519","type":"journal-article","created":{"date-parts":[[2015,6,15]],"date-time":"2015-06-15T09:37:15Z","timestamp":1434361035000},"page":"60-73","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":87,"title":["<scp>JAK<\/scp>\n                    inhibition induces silencing of T Helper cytokine secretion and a profound reduction in T regulatory cells"],"prefix":"10.1111","volume":"171","author":[{"given":"Clodagh","family":"Keohane","sequence":"first","affiliation":[{"name":"Department of Haematology Guy's and St Thomas\u2019 NHS Foundation Trust London UK"},{"name":"Department of Haematological Medicine Kings College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shahram","family":"Kordasti","sequence":"additional","affiliation":[{"name":"Department of Haematological Medicine Kings College London London UK"},{"name":"Department of Haematological Medicine Kings College Hospital NHS Foundation Trust London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Seidl","sequence":"additional","affiliation":[{"name":"Department of Haematological Medicine Kings College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pilar","family":"Perez Abellan","sequence":"additional","affiliation":[{"name":"Department of Haematological Medicine Kings College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas S. 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